Overexpression of microRNA‑96 is associated with poor prognosis and promotes proliferation, migration and invasion in cholangiocarcinoma cells via MTSS1

Yin, Xiaolan; Chai, Zong‐Tao; Sun, Xiaoting; Jin, Chen; Wu, Xiaoqing; Yang, Liying; Zhou, Xia; Liu, Feng

doi:10.3892/etm.2020.8502

Cited by 5 publications

(7 citation statements)

References 40 publications

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Section: Introductionmentioning

confidence: 99%

“…Evidence indicates that some miRNAs function as oncogenes or tumor suppressors along with influencing various biological processes, such as cell proliferation, migration, invasion, differentiation, and apoptosis, especially in cancer cells (Yin et al, 2020). Promising results have been observed in the treatment of several neoplasms after using circulating miRNAs as predictors (Yin et al, 2020). The identification of molecular alterations in miRNAs and candidate genes for CCA biomarkers may contribute to clarify the molecular mechanisms involved in the pathogenesis of CCA, thus assisting with the early diagnosis of the disease and choosing new therapeutic interventions.…”

Section: Introductionmentioning

confidence: 99%

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Investigating VEGF. miR-145-3p, and miR-101-3p Expression in Patients with Cholangiocarcinoma

Calastri

Ferreira

Tenani

et al. 2022

Asian Pac J Cancer Prev

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Introduction: Cholangiocarcinoma (CCA) is the second most common type of primary liver cancer. Several factors, such as epigenetic changes in promoter genes, gene expression, and microRNAs (miR), can contribute to genomic instability in cancer. This study aimed at evaluating the expression of VEGF, miRs 145-3p, and 101-3p in patients with CCA and their potential as biomarkers for diagnosis and prognosis of CCA. Material and methods : Sixty two patients were studied. Out of these 62 patients, 41 cases had confirm CCA and 21 cases had hepatopathies complications. The RNA was extracted from a paraffined tissue block, and then the synthesis of cDNA was performed. The analysis of the expression of VEGF, miR-145-3p, and miR-101-3p was carried out by polymerase chain reaction in real time. Results:The findings revealed that miRs 145-3p and 101-3p were under expressed in the case group compared to the control group (0.46; 0.17; P = 0.0001, respectively). VEGF was overexpressed in the case group compared to the control group (11.8; P = 0.0001). An increase in miR-145-3p expression level was observed in patients with perihilar CCA compared to those with distal CCA (0.51 ± 0.41; 0.17 ± 0.13; P = 0.0698). Survival rate analysis showed that 41.9% of patients with intrahepatic CCA and 31.5% of patients with extrahepatic CCA were free from death within 11 months, leading to a significant difference (P> 0.05). Conclusion: The underexpression of miRNAs, tumor suppressors, the overexpression of VEGF, smoking, and aging were associated with CCA based on our findings. It seems that the reduced expression of the studies miRNAs and increased expression of VEGF can contribute to a decrease in survival rate of patients with tumor in their intrahepatic bile ducts.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Investigating VEGF. miR-145-3p, and miR-101-3p Expression in Patients with Cholangiocarcinoma

Calastri

Ferreira

Tenani

et al. 2022

Asian Pac J Cancer Prev

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“…It has been reported that miR-96-5p may bind to MTSS1. MiR-96 was upregulated in cholangiocarcinoma and positively associated with poor prognosis; its upregulation may promote cholangiocarcinoma cell proliferation, migration and invasion by targeting MTSS1 [ 49 ]. miR-96 has also been reported to be increased in breast cancer; its overexpression may suppress breast cancer cell migration by downregulating the expression of MTSS1 [ 50 ].…”

Section: Discussionmentioning

confidence: 99%

circFBXO7/miR-96-5p/MTSS1 axis is an important regulator in the Wnt signaling pathway in ovarian cancer

Qiu

Zhou

et al. 2022

Mol Cancer

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Background CircRNAs are a novel class of evolutionarily conserved noncoding RNA molecules that form covalently closed continuous loop structures without 5′ caps and 3′ poly(A) tails. Accumulating evidence suggests that circRNAs play important regulatory roles in cancer and are promising biomarkers for cancer diagnosis and prognosis, as well as targets for cancer therapy. In this study, we identify and explore the role of a novel circRNA, circFBXO7, in ovarian cancer. Methods rRNA-depleted RNA-sequencing was performed to identify differentially expressed circRNAs between ovarian cancerous and normal tissues. qRT-PCR and single-molecule RNA in-situ hybridization was used to quantify circFBXO7 expression in tumor tissues. The association of circFBXO7 expression with patient prognosis was evaluated by Kaplan–Meier survival analysis. The biological function of circFBXO7 was also investigated using loss-of-function and gain-of-function assays in vivo and in vitro. Luciferase reporter and TOP/FOP-Flash reporter assays were then conducted together with RNA immunoprecipitation and western blot to assess the circFBXO7/miR-96-5p/MTSS1/Wnt/β-catenin axis. Results circFBXO7 was downregulated in ovarian cancer which was associated with poor prognosis. Biologically, circFBXO7 overexpression significantly suppressed ovarian cancer cell proliferation, migration, and invasion in vitro, and inhibited tumor growth and metastasis in vivo, whereas its knockdown exerted an opposite role. Mechanistically, circFBXO7 functioned as a competing endogenous RNA for miR-96-5p to regulate the expression of MTSS1. Consequently, downregulation of MTSS1 led to excessive accumulation of β-catenin and increased phosphorylation of GSK3β, leading to the translocation of β-catenin to the nucleus, thereby activating the Wnt/β-catenin signaling pathway and ultimately promoting ovarian cancer progression. Conclusions Our findings indicate that circFBXO7 acts as a bone fide tumor suppressor in ovarian cancer and that the circFBXO7/miR-96-5p/MTSS1 axis is an important regulator in the Wnt/β-catenin signaling pathway which may provide a promising target for ovarian cancer therapy.

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“…Significant downregulation of miR‐215 was recorded in breast cancer tissues and cell lines 10 . On the other hand, miR‐96 oncogenic effect on breast cancer was elucidated via its role in promoting breast cancer cell proliferation, migration by silencing PTPN9 expression in an in vitro and in vivo studies 11 . Over expression of miR‐96 directly impaired cell apoptotic responsiveness by repressing FoxO1 expression 12 .…”

Section: Introductionmentioning

confidence: 99%

“…10 On the other hand, miR-96 oncogenic effect on breast cancer was elucidated via its role in promoting breast cancer cell proliferation, migration by silencing PTPN9 expression in an in vitro and in vivo studies. 11 Over expression of miR-96 directly impaired cell apoptotic responsiveness by repressing FoxO1 expression. 12 This study aims to elucidate the signaling cascade of M. on ceasing proliferation, survival and metastasis of experimentally induced Ehrlich solid tumor as a model of adenocarcinoma.…”

Section: Introductionmentioning

confidence: 99%

Melatonin: A regulator of the interplay between FoxO1, miR96, and miR215 signaling to diminish the growth, survival, and metastasis of murine adenocarcinoma

et al. 2021

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Melatonin (Mel.), also known as the magic hormone, is a nocturnally secreted hormone orchestrates the clearance of free radicals that have been built up and cumulated during day. This study aims to detect the impact of pineal gland removal on the incidence of tumor development and to assess the signaling pathways via which exogenous melatonin counteract cancer growth. This goal has been achieved by novel approach for pineal destruction using dental micromotor which validated by melatonin downregulation in blood plasma. Mice were injected sub-cutenously with Ehrlich cells to develop solid tumor as a murine model of breast cancer. The increase at tumor markers carcino embryonic antigen, TNFα, and nuclear factor kappalight-chain-enhancer of activated B cells was over countered by exogenous melatonin supplementation (20 mg/kg) daily for 1 month. The anticancer effects of melatonin were significantly mediated by scavenging H 2 O 2 and NO and diminishing of lipid peroxidation marker malondialdehyde. The realtime polymerase chain Rx analyses indicated a significant effect of Melatonin in upregulating the expression of miR215, fork head box protein O1 (foxO1), and downregulation of miR96. Flowcytometric analyses indicated a significant effect of melatonin on induction of cell cycle arrest at G1 phase which was further confirmed by Ki67 downregulation. Immunohistochemical analyses indicated the role of melatonin in upregulating P53-dependent apoptosis and downregulating CD44 signaling for survivin, matrix metallo-protein kinase 2, and vascular endothelial growth factor to inhibit cell survival and metastasis. In conclusion, this study sheds the light on M./P53/miR215/ CD44 with an emphasis on M./miR96//foxO1 signaling cascades, as a novel

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Overexpression of microRNA‑96 is associated with poor prognosis and promotes proliferation, migration and invasion in cholangiocarcinoma cells via MTSS1

Cited by 5 publications

References 40 publications

Investigating VEGF. miR-145-3p, and miR-101-3p Expression in Patients with Cholangiocarcinoma

Investigating VEGF. miR-145-3p, and miR-101-3p Expression in Patients with Cholangiocarcinoma

circFBXO7/miR-96-5p/MTSS1 axis is an important regulator in the Wnt signaling pathway in ovarian cancer

Melatonin: A regulator of the interplay between FoxO1, miR96, and miR215 signaling to diminish the growth, survival, and metastasis of murine adenocarcinoma

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