Epigenetic disorders such as point mutations in cellular tumor suppressor genes, DNA methylation and post-translational modifications are needed to transformation of normal cells into cancer cells. These events result in alterations in critical pathways responsible for maintaining the normal cellular homeostasis, triggering to an inflammatory response which can lead the development of cancer. The inflammatory response is a universal defense mechanism activated in response to an injury tissue, of any nature, that involves both innate and adaptive immune responses, through the collective action of a variety of soluble mediators. Many inflammatory signaling pathways are activated in several types of cancer, linking chronic inflammation to tumorigenesis process. Thus, Inflammatory responses play decisive roles at different stages of tumor development, including initiation, promotion, growth, invasion, and metastasis, affecting also the immune surveillance. Immune cells that infiltrate tumors engage in an extensive and dynamic crosstalk with cancer cells, and some of the molecular events that mediate this dialog have been revealed. A range of inflammation mediators, including cytokines, chemokines, free radicals, prostaglandins, growth and transcription factors, microRNAs, and enzymes as, cyclooxygenase and matrix metalloproteinase, collectively acts to create a favorable microenvironment for the development of tumors. In this review are presented the main mediators of the inflammatory response and discussed the likely mechanisms through which, they interact with each other to create a condition favorable to development of cancer.
Cancer cells have accelerated metabolism and high glucose requirements. The up-regulation of specific glucose transporters may represent a key mechanism by which malignant cells may achieve increased glucose uptake to support the high rate of glycolysis. In present study we analyzed the mRNA and protein expression of GLUT1 and GLUT3 glucose transporters by quantitative real-time polymerase chain reaction (Q-PCR) and Western blotting technique in 76 cases of endometrial carcinoma and 70 cases of breast carcinoma. SLC2A1 and SLCA2A3 mRNAs expression was found, respectively in 100% and 97.4% samples of endometrial cancers and only in 50% and 40% samples of breast cancers. In endometrial cancers GLUT1 and GLUT3 protein expression was identified in 67.1% and 30.3% of cases. Analogously, in breast cancers in 48.7% and 21% of samples, respectively. The results showed that both endometrial and breast poorly differentiated tumors (grade 2 and 3) had significantly higher GLUT1 and GLUT3 expression than well-differentiated tumors (grade 1). Statistically significant association was found between SLCA2A3 mRNA expression and estrogen and progesterone receptors status in breast cancers. GLUT1 has been reported to be involved in the uptake of glucose by endometrial and breast carcinoma cells earlier and the present study determined that GLUT3 expression is also involved. GLUT1 and GLUT3 seem to be important markers in endometrial and breast tumors differentiation.
Long noncoding RNA (lncRNA) have been reported to modulate oncogenesis and be used to be target for tumor. The role of lncRNA NEAT1 (nuclear paraspeckle assembly transcript 1, Gene ID: 283131) in colorectal cancer (CRC) keeps unknown. This work was to investigate the pattern of lncRNA NEAT1 (NEAT1) expression in CRC and its functional value and biological significance. NEAT1 expression was analyzed in 56 cancer tissues and cell lines in CRC cases. Results showed that NEAT1 was significantly overexpressed in CRC cells and tissues. Clinicpathologic detection verified that high NEAT1 expression associated with bulk in CRC. The serum contents of NEAT1 were observably elevated comparing with healthy cases (P < 0.05). The levels of NEAT1 were elevated in distinguishing CRC from normal (ROCAUC = 0.9471; P < 0.01). Moreover, Kaplan-Meier analysis found that NEAT1 elevation led to adverse survival (P < 0.05). Further experiments illustrated that of NEAT1 knockdown signally inhibited growth and facilitated apoptosis. Importantly, we confirmed that Akt signaling pathway was inactivated after loss of NEAT1 in CRC. Taken together, this work support the first evidence that NEAT1 can be used to be a promising biomarker and target for novel treatment for human CRC.
Cells that migrate away from a central tumour into brain tissue are responsible for inefficient glioblastoma treatment. This migratory behaviour depends partially on lysosomal cysteine cathepsins. Reportedly, the expression of cathepsins B, L and S gradually increases in the progression from benign astrocytoma to the malignant glioblastoma, although their specific roles in glioma progression have not been revealed. The aim of this study was to clarify their specific contribution to glioblastoma cell invasion. The differences between the matrix invading cells and non-invading core cells from spheroids derived from glioblastoma cell culture and from glioblastoma patients’ biopsies, and embedded in type I collagen, have been studied at the mRNA, protein and cathepsin activity levels. Analyses of the two types of cells showed that the three cathepsins were up-regulated post-translationally, their specific activities increasing in the invading cells. The cystatin levels were also differentially altered, resulting in higher ratio of cathepsins B and L to stefin B in the invading cells. However, using specific synthetic inhibitors and silencing strategies revealed that only cathepsin B activity was involved in the invasion of glioblastoma cells, confirming previous notion of cathepsin B as tumour invasiveness biomarker. Our data support the concept of specific roles of cysteine cathepsins in cancer progression. Finally the study points out on the complexity of protease regulation and the need to include functional proteomics in the systems biology approaches to understand the processes associated with glioma invasion and progression.
The investigation of prognostic factor for gastric cancer is still desirable because of dismal prognosis in gastric cancer. Lauren’s classification is currently a useful histological classification. There are few large series evaluating the prognostic significance of Lauren’s classification in gastric cancer. From January 1987 to December 2013, a total of 3071 patients received gastrectomy for gastric cancer. According Lauren’s classification, 1423(46.3 %) patients were intestinal type, 1000 patients (32.6 %) were diffuse type, and 648 patients (21.1 %) were mixed type. The clinicopathological characteristics and prognosis in Lauren’s classification were analyzed in these patients. Our results showed that patients with intestinal type gastric cancer (57.7 %) had a better 5-year overall survival than diffuse type (45.6 %) and mixed type (43.4 %, P < 0.001). The clinicopathological characteristics showed that gastric cancer patients with intestinal type were older (P < 0.001), male predominant (P < 0.001), smaller tumor size (P < 0.001), distal stomach predominant (P < 0.001), relative well differentiated (P < 0.001), less advanced Borrmann type (P < 0.001), less scirrhous type stromal reaction(P < 0.001), less infiltrating type of Ming’s histology type(P < 0.001), less tumor invasion depth and less lymphovascular invasion (P < 0.001). Multivariate analysis with overall survival as an endpoint showed that age (P = 0.005), Borrmann classification (P < 0.001), pathological T category (P = 0.023), pathological N category (P < 0.001) and Lauren’s classification (P = 0.003) were significant correlated in gastric cancer. Lauren’s classification is an independent prognostic factor in gastric cancer patient undergoing gastrectomy. Lauren’s classification can serve as a prognostic marker for gastric cancer patient receiving gastrectomy. The clinicopathological appearance and prognosis of mixed type gastric cancer is similar to diffuse type gastric cancer.
Gastric cancer (GC) is the most common solid tumor in digestive system. Nuclear-enriched abundant transcript 1 (NEAT1) gene is a lncRNA, and reveal potential oncogene role in several malignant tumors. The aim of this study is to investigate the expression and clinical significance of Nuclear Paraspeckle Assembly Transcript 1 (NEAT1) gene and its influence to malignant biologic behaviors and chemotherapy resistance to adriamycin in GC. This study found NEAT1 was up-regulated in GC tissues and cells, especially in in GC adriamycin-resistant cells. NEAT1 silence in SGC7901 cells could inhibit proliferation and invasion ability, and promote cell apoptosis significantly. NEAT1 silence in adriamycin-resistant SGC7901/ADR cells also depressed the half maximal inhibitory concentration (IC50) for adriamycin, chemotherapy resistance to adriamycin was inhibited significantly. NEAT1 knockdown promoted apoptosis in SGC7901/ADR cells induced by adriamycin. In summary, lncRNA NEAT1 is high-expressed in GC and functions as an oncogene to modulate apoptosis, invasion, proliferation and chemotherapy resistance of GC cells, which might be a novel potential therapeutic target for GC.
Long Non-coding RNAs (lncRNAs) refer to all non-protein coding transcripts longer than 200 nucleotides. Their critical roles in different biological pathways have been already well established. Altered expression of lncRNAs can be involved in the cancer initiation and/or progression. Since patients with hepatocellular carcinoma (HCC) are usually diagnosed in late stages, developing diagnostic methods seems to be essential. In this study, the expression levels of different lncRNAs were systematically analysed in different genomic and transcriptome datasets. The analyses showed that SNHG6 is among the lncRNAs with distinctive dysregulation of expression and copy number variation in HCC tumors compared with normal tissues. The results also suggest that the dysregulation of SNHG6 is highly cancer type specific. Through co-occurrence analyses, we found that SNHG6 and its related co-expressed genes on 8q are involved in the structural integrity of ribosome and translation. This comprehensive in silico analysis, provides a resource for investigating SNHG6 in hepatocellular carcinoma and lays the groundwork for design of next researches.
MicroRNAs (miRNAs) are a group of small non-coding RNA molecules predicted to control the activity of about 30 % of all protein-coding genes in mammals. The expression of microRNA-424-5p (miR-424-5p) has been shown to vary in multiple hematological and solid organ malignancies, such as pancreatic cancer. This study aimed to characterize the function of upregulated miR-424-5p in pancreatic cancer and show how downstream suppressor of cytokine-induced signaling 6 (SOCS6) is negatively regulated by miR-424-5p. MiR-424-5p and SOCS6 expression was detected using quantitative real-time PCR (qRT-PCR) in pancreatic cancer tissues and adjacent non-tumorous ductal epithelium tissues. Luciferase reporter assays were used to assess SOCS6 as a target of miR-424-5p. The downstream effect of SOCS6 was measured by qRT-PCR after miR-424-5p inhibition and SOCS6 upregulation. The functions of miR-424-5p in vitro in pancreatic cancer cells were measured by migration and invasion assays and flow cytometry. Results suggested miR-424-5p was significantly upregulated in pancreatic cancer and suppress the expression of SOCS6, and miR-424-5p increased proliferation, migration and invasion of pancreatic cancer cells, while inhibited cell apoptosis. It was concluded that miR-424-5p is frequently upregulated in pancreatic cancer and modulates ERK1/2 signaling pathway by negatively regulating SOCS6.
Search for new substances with antiproliferative activity and apoptosis inducing potential towards HepG2 cells is important since HCC is notoriously resistant to conventional chemotherapy. Dietary phytochemicals with significant anti-proliferative and apoptosis inducing potential are considered as agents promising for cancer therapy. Naringenin, a common dietary flavonoid abundantly present in fruits and vegetables, is believed to possess strong cytotoxic activity in numerous types of cancer cells. However, the detailed molecular mechanisms of its antiproliferative effects and apoptosis induction are still unclear. In this study, we investigated antiproliferative and apoptosis-inducing effect of naringenin in human hepatocellular carcinoma HepG2 cells. Naringenin was shown to inhibit the proliferation of HepG2 cells resulted partly from an accumulation of cells in the G0/G1 and G2/M phase of the cell cycle. Naringenin induced a rapid accumulation of p53, which might account for the naringenin-induced G0/G1 and G2/M phase arrests in Hep G2 cells. In addition, naringenin have been shown to induce apoptosis as evidenced by nuclei damage and increased proportion of apoptotic cells detected by flow cytometry analysis. Naringenin triggered the mitochondrial-mediated apoptosis pathway as shown by an increased ratio of Bax/Bcl-2, subsequent release of cytochrome C, and sequential activation of caspase-3. Our results showed that naringenin had inhibitory effect on the growth of HepG2 cell line through inhibition of cell proliferation and apoptosis induction. The elucidation of the drug targets of naringenin on inhibition of tumor cells growth should enable further development of naringenin for liver cancer therapy.
Prostate-specific membrane antigen (PSMA) is a transmembrane protein that is overexpressed in advanced stage prostate adenocarcinomas. As a novel target for in vivo prognostic and therapeutic approaches, the distribution pattern of PSMA in primary and metastatic tumors is of significant interest. In this study we addressed the cellular distribution and heterogeneity of PSMA expression. Paraffin-embedded sections of 51 patients with primary prostate carcinoma and distant metastases were evaluated. Immunohistochemistry was used to determine the cellular localization, staining intensity and positive cell fraction which were related to tumor type and growth pattern. We demonstrated differences in the intracellular localization of the PSMA immunostaining which seem to be related to the tumor differentiation pattern. A significant number of the primary tumors (7/51) and metastases (6/51) presented with highly heterogeneous PSMA expression and in further 2 primary, and 8 metastatic tumors the staining was in the negative range (<10% positive tumor cells). A direct correlation between histological parameters and PSMA expression could not be demonstrated. Our findings clearly support the feasibility but also direct to potential failures of PSMA-targeted in vivo diagnostic and therapeutic approaches in prostate cancer patients with distant metastasis.
The PI3K/AKT/mTOR pathway plays a crucial role in the regulation of multiple cellular functions including cell growth, proliferation, metabolism and angiogenesis. Emerging evidence has shown that deregulation of this pathway has a role promoting gastric cancer (GC). The aim was to assess the expression of genes involved in this pathway by qPCR in 23 tumor and 23 non-tumor gastric mucosa samples from advanced GC patients, and in AGS, MKN28 and MKN45 gastric cancer cell lines. Results showed a slight overexpression of PIK3CA, PIK3CB, AKT1, MTOR, RPS6KB1, EIF4EBP1 and EIF4E genes, and a slightly decreased PTEN and TSC1 expression. In AGS, MKN28 and MKN45 cells a significant gene overexpression of PIK3CA, PIK3CB, AKT1, MTOR, RPS6KB1 and EIF4E, and a significant repression of PTEN gene expression were observed. Immunoblotting showed that PI3K-β, AKT, p-AKT, PTEN, mTOR, p-mTOR, P70S6K1, p-P70S6K1, 4E-BP1, p-4E-BP1, eIF4E and p-eIF4E proteins were present in cell lines at different levels, confirming activation of this pathway in vitro. This is the first time this extensive panel of 9 genes within PI3K/AKT/mTOR pathway has been studied in GC to clarify the biological role of this pathway in GC and develop new strategies for this malignancy.
MicroRNA-21 (miR-21) is overexpressed in a wide variety of cancers and has been related to cellular proliferation, apoptosis, and invasion; however, the function of miR-21 is unknown in oral tongue squamous cell carcinoma (OTSCC). The purpose of this study was to examine miR-21 expression in OTSCC, correlate it with clinicopathological factors, and investigate its contribution to OTSCC cell invasion. MiR-21 expression in 79 primary OTSCCs was evaluated using locked nucleic acid in situ hybridization, and correlation was examined with the clinicopathological factors. To determine the miR-21 target, we searched for molecular genes involved in tumor invasion using the commonly cited prediction program miRanda. In an OTSCC cell line, SCC25 cells, we further evaluated whether miR-21 contributes to cell invasiveness by blocking its expression with a specific knockdown LNA probe and confirmed the direct target by Matrigel invasion assay and Western blotting. MiR-21 overexpression was detected in 60 of 79 cases (75.9 %) and correlated with the pattern of invasion (P = 0.016). We selected DKK2 as a Wnt/antagonist involved in tumor invasion. MiR-21 overexpression was significantly correlated with the DKK2-/β-catenin- immunohistochemical phenotype. Knockdown of miR-21 significantly decreased the invasion potential of SCC25 cells with up-regulated DKK2. It was found that miR-21 is overexpressed and associated with tumor invasion in OTSCC, and that miR-21 promotes OTSCC cell invasion via the Wnt/β-catenin pathway by targeting DKK2 in vitro. These results suggest that miR-21 may be a potential therapeutic target for OTSCC treatment.
Elevated expression of MALAT-1 was found in various cancers, and correlated with metastasis and prognostic. This meta-analysis collected all relevant articles and explored correlation of MALAT-1 with lymph node metastasis (LNM), distant metastasis (DM), and overall survival (OS). A quantitative meta-analysis was performed through a systematic search in PubMed, Web of Science, Medline, CNKI, CBM, and the Cochrane Library. The odds ratios (OR) of LNM and DM and hazard ratio (HR) of OS were calculated to assess the association strength. Eight studies with a total of 845 patients were included in the meta-analysis. Six different types of cancer were evaluated, with 2 non-small cell lung cancer (NSCLC), 1 colorectal cancer (CRC), 1 gastric cancer (GC), 2 pancreatic cancer (PC), 1 clear cell renal cell carcinoma (ccRCC), and 1 osteosarcoma (OSA). Compared with low MALAT-1 expression, high MALAT-1 expression correlated with more LNM (OR = 2.08, 95 %CI: 1.00-4.32, p = 0.05) by a random-effects model (I 2 = 71 %, p = 0.004). A similar result was seen between MALAT-1 expression and DM, the OR was 3.52 (95 %CI: 1.06–11.71, p = 0.04) adopting a random-effects model (I 2 = 59 %, p = 0.04). Additionally, our analysis showed a poorer OS in patients with high MALAT-1 expression than those with low MALAT-1 expression (HR = 2.12, 95 %CI: 1.60–2.82, p < 0.001) adopting a random-effects model (I 2 = 56 %, p = 0.04). MALAT-1 may serve as a molecular marker for cancer metastasis and prognosis.
MicroRNAs (miRNAs) have been found to play a critical role in colorectal adenoma-carcinoma sequence. MiRNA-specific high-throughput arrays became available to detect promising miRNA expression alterations even in biological fluids, such as plasma samples, where miRNAs are stable. The purpose of this study was to identify circulating miRNAs showing altered expression between normal colonic (N), tubular adenoma (ADT), tubulovillous adenoma (ADTV) and colorectal cancer (CRC) matched plasma and tissue samples. Sixteen peripheral plasma and matched tissue biopsy samples (N n = 4; ADT n = 4; ADTV n = 4; CRC n = 4) were selected, and total RNA including miRNA fraction was isolated. MiRNAs from plasma samples were extracted using QIAamp Circulating Nucleic Acid Kit (Qiagen). Matched tissue-plasma miRNA microarray experiments were conducted by GeneChip® miRNA 3.0 Array (Affymetrix). RT-qPCR (microRNA Ready-to-use PCR Human Panel I + II; Exiqon) was used for validation. Characteristic miRNA expression alterations were observed in comparison of AD and CRC groups (miR-149*, miR-3196, miR-4687) in plasma samples. In the N vs. CRC comparison, significant overexpression of miR-612, miR-1296, miR-933, miR-937 and miR-1207 was detected by RT-PCR (p < 0.05). Similar expression pattern of these miRNAs were observed using microarray in tissue pairs, as well. Although miRNAs were also found in circulatory system in a lower concentration compared to tissues, expression patterns slightly overlapped between tissue and plasma samples. Detected circulating miRNA alterations may originate not only from the primer tumor but from other cell types including immune cells.
Studies have investigated the effect of ROBO1. All the same, the relationship between miR-490-5p and ROBO1, and the underlying mechanism are still unclear. We aimed to study the effect of microRNA-490-5p (miR-490-5p) on hepatocellular carcinoma (HCC) cell proliferation, migration and invasion by directly regulating ROBO1. The expression of miR-490-5p and ROBO1 in HCC tissues and cells were tested by RT-qPCR, and the Hep3B cells were selected for subsequent experiments. We confirmed the relationship between miR-490-5p and ROBO1 by luciferase reporter system. The effects of miR-490-5p on cell proliferation, migration and invasion of Hep3B cells were assessed by MTT assay, colony formation assay, wound healing assay and transwell assay, respectively. Flow cytometry was employed to detect the influence of miR-490-5p on cell cycle and apoptosis of Hep3B cells. The expression of miR-490-5p was down-regulated, while ROBO1 was up-regulated in HCC tissues and cells than the controls. MiR-490-5p can target ROBO1. MiR-490-5p inhibited cell proliferation, migration and invasion, but promoted cell apoptosis of Hep3B cells by inhibiting ROBO1. We confirmed that miR-490-5p could directly suppress ROBO1, which might be a potential mechanism in inhibiting HCC cell proliferation, migration and invasion.
Beta-glucans are widely used in treatment, cosmetics, and the food industry. Glucans play a significant role in activation of the immune and antioxidant system and inhibiting tumor proliferation. In the current study the antitumor activities of new high and low molecular weight beta-glucan derived from oats were investigated in two human lung cancer cell line (A549, H69AR) and normal keratinocytes (HaCaT). The effect of high and low molecular weight beta-glucan from oat was evaluated by cellular viability assessment, lipid peroxidation and manganese superoxide dismutase evaluation and cytoskeleton visualisation. Additionally the level of red blood cells hemolysis was performed. Our results indicate strong anti-tumor properties of new beta-glucan from oat and at the same time no toxicity for normal cells.
Gastric cancer (GC) is one of the mostly terminal malignancies with poor prognosis. Long noncoding RNA EGOT (EGOT) acts as a crucial regulator in the breast cancer. However, the function of EGOT in GC remains unknown. This work was to explore the clinical value and biological significance of EGOT in GC. EGOT levels in GC tissue and cell were analyzed by qRT–PCR. After knockdown of EGOT, GC cell growth and cycle progression were detected. The expression of EGOT was observably elevated in GC. Upregulation of EGOT was related with lymphatic metastasis and TNM stage. In addition, knockdown of EGOT by siRNA could significantly inhibit GC cell proliferation and arrest cycle progression in G1 phase. Moreover, EGOT mediated cyclin D1 expression in GC cells which was regulated by Hedgehog pathway. Further, loss of EGOT downregulated Hedgehog signaling pathway in GC cells. EGOT functions as an oncogene in GC, and may be useful as a conceivable diagnostic and prognostic biomarker for GC tumorigenesis.
Astrocytic gliomas are the most common type of human primary brain tumors with poor prognosis. MicroRNAs(miRs) are frequently deregulated in gliomas and play an oncogenic or tumor suppressor role. In our previous study we found that miR-19a and miR-19b were up-regulated in malignant glioma cell lines by microRNA array. For further validation of this finding, the expression of miR-19a and miR-19b was detected by qRT-PCR and in situ hybridization(ISH) in 8 malignant glioma cell lines, 43 freshly resected glioma samples and 75 archival paraffin embedded glioma specimens with different grades of malignancy in the present study. The results demonstrate that miR-19a and miR-19b are overexpressed in glioma cell lines and astrocytic glioma tissues, and their expression level is positively correlated with tumor grades. Additionally, the tumor suppressor gene PTEN is identified as the target of miR-19a and miR-19b by Luciferase assay. It is speculated that miR-19a and miR-19b may have an oncogenic role in gliomagenesis at least partially via the negative regulation of PTEN and the molecular mechanism of gliomagenesis in which miR 19a and miR-19b involved should be investigated further.
A host of studies have revealed that long non-coding RNAs (lncRNAs) are critically involved in the development and progression of epithelial ovarian cancer. LncRNA TUBA4B is recently identified to be a critical mediator in non-small cell lung cancer. However, the clinical roles and biological functions of lncRNA TUBA4B in epithelial ovarian cancer have yet to be fully clarified. The present study was conducted to explore the expression of lncRNA TUBA4B in human epithelial ovarian cancer tissues and potential roles of lncRNA TUBA4B in ovarian cancer cells. The matched epithelial ovarian cancer specimens and adjacent normal tissues were employed to detect the expression of lncRNA TUBA4B. The prognostic value of lncRNA TUBA4B for tumor progression and survival rate was investigated. The effects of lncRNA TUBA4B on ovarian cancer cell proliferation and migration were also explored. The expression of lncRNA TUBA4B was significantly decreased in epithelial ovarian cancer tissue specimens. The low lncRNA TUBA4B level was closely related with pathological grade, FIGO stage and lymph node metastases, and serum CA125 level. Enforced expression of lncRNA TUBA4B obviously reduced the proliferation of SKOV3 cells, and attenuated the activation of ERK and Akt signaling pathways. Our data demonstrate for the first time that lower lncRNA TUBA4B may be a novel independent prognostic biomarker for overall survival of epithelial ovarian cancer. Overexpression of lncRNA TUBA4B inhibits the proliferation of ovarian cancer cells. LncRNA TUBA4B may be an important target for therapeutic intervention in ovarian cancer.
MicroRNAs (miRNAs) are small non-coding RNAs composed of 18–25 nucleotides that can post-transcriptionally regulate gene expression and have key regulatory roles in cancer, acting as both oncogenes and tumor suppressors. About 1000 genes in humans encode miRNAs, which account for approximately 3% of the human genome, and up to 30% of human protein coding genes may be regulated by miRNAs. The objective of this article is to evaluate the expression profile of four miRNAs previously implicated in triple negative breast cancer: miR-10b, miR-26a, miR-146a and miR-153, and to determine their possible interaction in triple negative and non triple negative breast cancer based on clinical outcome and the expression of BRCA1. 24 triple-negative and 13 non triple negative breast cancer cases, were studied by q-RT-PCR and immunohistochemistry to determine the expression of the four studied miRNAs and the BRCA1 protein, respectively. We observed that the BRCA1 protein was absent in 62.5% of the triple negative cases. Besides, the miR-146a and miR-26a were over expressed in triple negative breast cancer. These two miRNAs, miR-10b and miR-153 were significantly associated to lymph node metastases occurrence in triple negative breast carcinoma. All the analyzed microRNAs were not associated with the expression of BRCA1 in our conditions. Our work provides evidence that miR-146a, miR-26a, miR-10b and miR-153 could be defined as biomarkers in triple negative breast cancer to predict lymph node metastases (LNM).