NT21MP negatively regulates paclitaxel-resistant cells by targeting miR‑155‑3p and miR‑155-5p via the CXCR4 pathway in breast cancer

Wang, Yueyue; Liu, Yan; Zhang, Lingyu; Xu, Huijing; Chen, Tiantian; Yu, Li; Wang, Haifeng; Chen, Sulian; Wang, Wenrui; Chen, Changjie; Yang, Qingling

doi:10.3892/ijo.2018.4477

“…Furthermore, miR-155 directly targeted and inhibited a series of genes (e.g. FOXO3, SMARCA4 or Ubiquilin-1) to participate in the biological process of tumor development (37)(38)(39)(40). To the best of our knowledge, the present study was the first to indicate that TERF1 may be a direct target of miR-155, as confirmed by a dual luciferase reporter assay.…”

Section: Discussionsupporting

confidence: 65%

TERF1 downregulation promotes the migration and invasion of the PC3 prostate cancer cell line as a target of miR‑155

Chen

¹

,

He²,

Liang

³

et al. 2020

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Telomeric repeat binding factor 1 (TerF1) has been identified as a tumor suppressor gene in numerous types of human cancer. However, the expression of TERF1 and its mechanism in prostate cancer (PCa) remains unclear. The present study aimed to explore the expression and functions of TERF1 in PCa. The UALCAN database was used to analyze the differential expression of TERF1 between normal prostate tissue and primary PCa tissue. Cell apoptosis was analyzed by Annexin V/propidium iodide staining, and wound healing and Transwell assays were used to detect the cell migration and invasion abilities, respectively. The cell viability was analyzed using an MTT assay. Reverse transcription-quantitative PCR and western blotting were used to analyze the mRNA and protein expression levels, respectively, of epithelial-mesenchymal transition (EMT) markers following TERF1 knockdown in the PC3 cell line. A dual luciferase reporter assay was used to verify the association between TERF1 and microRNA (miR)-155 predicted by bioinformatics analysis. Rescue experiments were performed to determine the role of the miR-155/TERF1 axis in regulating the cellular behaviors of PCa. The results demonstrated that the expression levels of TERF1 in the primary prostate tumors were significantly downregulated compared with in prostate normal tissue. TERF1 silencing was discovered to significantly promote cell viability, migration and invasion, while suppressing cell apoptosis. The impact of TERF1 on PC3 cells was suggested to occur through the EMT pathway. TERF1 was confirmed to be the direct target of miR-155. The overexpression of miR-155 promoted the viability, migration and invasion, while suppressing the apoptosis of the PC3 cell line, while the knockdown of miR-155 in PC3 cells achieved the opposite trends. In addition, TERF1 overexpression reversed the promotive effects of upregulated miR-155 expression levels on the migration and apoptosis of PC3 cells. On the contrary, the knockdown of TERF1 reversed the migration and apoptosis abilities of the downregulated miR-155 expression levels on the cellular behaviors of PC3 cells. In conclusion, TERF1, as a direct target of miR-155, was discovered to be significantly downregulated in PCa, which was suggested to promote the migration and invasion of PCa via the EMT pathway.

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“…Previous studies have found that microRNA-155 is abnormally expressed in various tumors and plays a centrol role in the process of tumor initiation, progression, invasion, and metastasis [29][30][31][32][33][34][35] . Our results indicated that expression of microRNA-155 can be up-regulated in some patients of gastric cancer and down-regulated in others.…”

Section: Discussionmentioning

confidence: 99%

Clinical Significance of MicroRNA-155 Regulated Autophagy and Apoptosis by targeting gene Rictor/Fos in Gastric Cancer Progression

Chen

¹

,

Yu

²

,

Ren

³

et al. 2020

Preprint

Self Cite

3

0

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BACKGROUND Microrna-155 plays an important role in the pathogenesis, progression and treatment of various cancers. It is abnormally expressed in gastric cancer, but its expression level, mechanism and significance are controversial in different studies. So we make the study to explore the expression level, significance and mechanism of microRNA-155 on gastric cancer. METHODS Target genes of microRNA-155 in TargetScan and mirDB databases were analyzed by Wayne Mapping, Enrichr database, String database, TIMER database. Forty-three pairs of cancer tissues and adjacent tissues were collected to extract total RNA and protein. Expression of MicroRNA-155, Rictor, Fos, Beclin1, LC3, caspase3 and caspase9 were measured by qRT-PCR and western blot. The relationship between gene expression and clinicopathological factors were analyzed. SPSS 23.0 was used for statistical analysis. RESULTS A total of 700 (miRDB) and 556 (TargetScan) target genes were obtained and 280 genes were in the intersection of Wayne Mapping, 49 of them had a target score of 90 or more. GO and KEGG analysis revealed that they were related to autophagy or apoptosis pathway. Rictor and Fos were selected as research objects. Thirty-two cases showed high microRNA-155 expression (group H) and 11 cases showed low expression (group L). Twelve patients had high Rictor expression and 31 patients had low expression; Thirteen cases had roughly normal Fos expression and 30 cases had low or negative expression; Thirty-three cases had high Beclin1/LC3 expression and 10 cases had low expression; Ten cases had high caspase3/caspase9 expression and 33 cases had low expression. According to the results of immunohistochemistry and western blot, Rictor, Fos, caspase3 and caspase9 were low expressed while Beclin1 and LC3 were high expressed in group H. However, all the six genes had no significant difference in group L. CONCLUSIONS The abnormal expression of microRNA-155 may indicate the occurrence of gastric cancer and its expression level is negatively correlated with clinical stage of cancer. The down-regulated expression of Rictor and Fos, enhancement of autophagy and weakening of apoptosis may be related to the over-expression of microRNA-155. MicroRNA-155 may promote the progression of gastric cancer by promoting autophagy and inhibiting apoptosis.

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“…Previous studies have found that microRNA-155 is abnormally expressed in various tumors and plays a centrol role in the process of tumor initiation, progression, invasion, and metastasis [29][30][31][32][33][34][35] . Our results indicated that expression of microRNA-155 can be up-regulated in some patients of gastric cancer and down-regulated in others.…”

Section: Discussionmentioning

confidence: 99%

Clinical Significance of MicroRNA-155 Regulated Autophagy and Apoptosis by targeting gene Rictor/Fos in Gastric Cancer Progression

Chen

¹

,

Liu

²

,

Ren

³

et al. 2020

Preprint

Self Cite

0

View full text Add to dashboard Cite

BACKGROUND Microrna-155 plays an important role in the pathogenesis, progression and treatment of various cancers. It is abnormally expressed in gastric cancer, but its expression level, mechanism and significance are controversial in different studies. So we make the study to explore the expression level, significance and mechanism of microRNA-155 on gastric cancer. METHODS Target genes of microRNA-155 in TargetScan and mirDB databases were analyzed by Wayne Mapping, Enrichr database, String database, TIMER database. Forty-three pairs of cancer tissues and adjacent tissues were collected to extract total RNA and protein. Expression of MicroRNA-155, Rictor, Fos, Beclin1, LC3, caspase3 and caspase9 were measured by qRT-PCR and western blot. The relationship between gene expression and clinicopathological factors were analyzed. SPSS 23.0 was used for statistical analysis. RESULTS A total of 700 (miRDB) and 556 (TargetScan) target genes were obtained and 280 genes were in the intersection of Wayne Mapping, 49 of them had a target score of 90 or more. GO and KEGG analysis revealed that they were related to autophagy or apoptosis pathway. Rictor and Fos were selected as research objects. Thirty-two cases showed high microRNA-155 expression (group H) and 11 cases showed low expression (group L). Twelve patients had high Rictor expression and 31 patients had low expression; Thirteen cases had roughly normal Fos expression and 30 cases had low or negative expression; Thirty-three cases had high Beclin1/LC3 expression and 10 cases had low expression; Ten cases had high caspase3/caspase9 expression and 33 cases had low expression. According to the results of immunohistochemistry and western blot, Rictor, Fos, caspase3 and caspase9 were low expressed while Beclin1 and LC3 were high expressed in group H. However, all the six genes had no significant difference in group L. CONCLUSIONS The abnormal expression of microRNA-155 may indicate the occurrence of gastric cancer and its expression level is negatively correlated with clinical stage of cancer. The down-regulated expression of Rictor and Fos, enhancement of autophagy and weakening of apoptosis may be related to the over-expression of microRNA-155. MicroRNA-155 may promote the progression of gastric cancer by promoting autophagy and inhibiting apoptosis.

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NT21MP negatively regulates paclitaxel-resistant cells by targeting miR‑155‑3p and miR‑155-5p via the CXCR4 pathway in breast cancer

Cited by 9 publications

References 51 publications

TERF1 downregulation promotes the migration and invasion of the PC3 prostate cancer cell line as a target of miR‑155

TERF1 downregulation promotes the migration and invasion of the PC3 prostate cancer cell line as a target of miR‑155

Clinical Significance of MicroRNA-155 Regulated Autophagy and Apoptosis by targeting gene Rictor/Fos in Gastric Cancer Progression

Clinical Significance of MicroRNA-155 Regulated Autophagy and Apoptosis by targeting gene Rictor/Fos in Gastric Cancer Progression

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