miR-26a-5p suppresses tumor metastasis by regulating EMT and is associated with prognosis in HCC

Chang, Lei; Li, K; Guo, Tao

doi:10.1007/s12094-016-1582-1

Cited by 45 publications

(32 citation statements)

References 43 publications

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“…miRNAs have a critical role in the biological behavior of liver cancer (23). Various studies have indicated the effectiveness of miRNAs against HCC and HB is due to their ability to inhibit cell growth, invasion ability, angiogenesis and induce tumor cell apoptosis (24)(25)(26)(27). miR-378a has been reported to regulate multiple physiological activities, including myoblast differentiation, adipogenesis, and tumor growth (28), such as those found in colorectal cancer and rhabdomyosarcoma (19,(29)(30)(31).…”

Section: Discussionmentioning

confidence: 99%

miR‑378a enhances the sensitivity of liver cancer to sorafenib by targeting VEGFR, PDGFRβ and c‑Raf

Zhang

Pan³

et al. 2018

Mol Med Report

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Liver cancer is a globally prevalent cancer with poor prognosis. The present study investigated the link between microRNA-378a (miR‑378a) expression and the sensitivity of hepatocellular carcinoma (HCC) and hepatoblastoma (HB) cancers to sorafenib therapy. miR‑378a expression was determined in liver tissue samples from healthy candidates and patients with liver cancer using the reverse transcription‑quantitative polymerase chain reaction. The antitumor effects of miR‑378a alone and in combination with sorafenib were investigated in the HB cell line HepG2 and the HCC cell line SMMC‑7721 with methyl thiazoyl tetrazolium, colony formation, flow cytometry and Transwell migration assays. The underlying mechanisms were investigated using western blot analysis. miR‑378a expression was decreased in tissue samples from patients with liver cancer. HCC and HB cell line proliferation and invasion ability was inhibited by miR‑378a. The combination of miR‑378a and sorafenib provided the greatest inhibition. Western blot indicated that mitogen activated protein kinase signaling pathway proteins, vascular endothelial growth factor receptor, platelet derived growth factor receptor β, Raf‑1 proto‑oncogene, serine/threonine kinase and matrix metallopeptidase 2 were regulated by miR‑378a alone and to a greater extent when combined with sorafenib. Results suggest that miR‑378a can inhibit liver cancer cell growth and enhance the sensitivity of liver cancer cells to sorafenib‑based chemotherapies.

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Section: Discussionmentioning

confidence: 99%

miR‑378a enhances the sensitivity of liver cancer to sorafenib by targeting VEGFR, PDGFRβ and c‑Raf

Zhang

Pan³

et al. 2018

Mol Med Report

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“…Gao et al found that p53 mediated activation of miR-26a induced apoptosis in HCC cells [175]. Furthermore, low expression of miR-26a correlated with a poor prognosis of HCC patients [144,176]. This finding was also confirmed in patients with HBV-induced HCC [177].…”

Section: Microrna-26amentioning

confidence: 86%

“…However, in the same study, miR-26a promoted HCC tumor cell migration, invasion and metastasis in vivo after injection of tumor cells into the tail vein of nude mice, probably by downregulation of phosphatase and tensin homolog (PTEN) [150]. Other studies also showed that a low amount of miR-26a in HCC leads to activation of the Wnt/β-catenin pathway, reduced E-cadherin expression and induction of epithelial to mesenchymal transition (EMT) [144,145]. Therefore, in contrast to early cancer development, miR-26a might also have oncogenic functions in advanced tumor stages and metastasis in HCC and other types of cancer ( Figure 5).…”

Section: Microrna-26amentioning

confidence: 87%

“…Further, low miR-622 expression induces de-repression of MAP4K4 promoting epithelial to mesenchymal transition (EMT) and invasiveness [142,143]. Low levels of miR-26a in tumor cells lead to increased integrin α5 expression and reduced E-cadherin expression inducing EMT [144][145][146]. It further induces the release of anti-apoptotic SODD [147].…”

Section: The Let-7 Mirna Familymentioning

confidence: 99%

“…Another potent tumor-suppressive miRNA is the miR-26a, which is strongly downregulated in both melanoma [36,89,147,[167][168][169] and HCC [40,144,150,[170][171][172][173] (Figure 5). In melanoma, re-expression of miR-26a induced cell cycle arrest and increased apoptosis [167,174].…”

Section: Microrna-26amentioning

confidence: 99%

See 2 more Smart Citations

Dissimilar Appearances Are Deceptive–Common microRNAs and Therapeutic Strategies in Liver Cancer and Melanoma

Linck-Paulus

Hellerbrand

Bosserhoff

et al. 2020

Cells

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In this review, we summarize the current knowledge on miRNAs as therapeutic targets in two cancer types that were frequently described to be driven by miRNAs—melanoma and hepatocellular carcinoma (HCC). By focusing on common microRNAs and associated pathways in these—at first sight—dissimilar cancer types, we aim at revealing similar molecular mechanisms that are evolved in microRNA-biology to drive cancer progression. Thereby, we also want to outlay potential novel therapeutic strategies. After providing a brief introduction to general miRNA biology and basic information about HCC and melanoma, this review depicts prominent examples of potent oncomiRs and tumor-suppressor miRNAs, which have been proven to drive diverse cancer types including melanoma and HCC. To develop and apply miRNA-based therapeutics for cancer treatment in the future, it is essential to understand how miRNA dysregulation evolves during malignant transformation. Therefore, we highlight important aspects such as genetic alterations, miRNA editing and transcriptional regulation based on concrete examples. Furthermore, we expand our illustration by focusing on miRNA-associated proteins as well as other regulators of miRNAs which could also provide therapeutic targets. Finally, design and delivery strategies of miRNA-associated therapeutic agents as well as potential drawbacks are discussed to address the question of how miRNAs might contribute to cancer therapy in the future.

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Critical role of miR‐26a‐5p/Wnt5a signaling in gambogic acid‐induced inhibition of gastric cancer

Zhang

Liang

Cao

2021

J Biochem & Molecular Tox

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Gastric cancer (GC) represents the fifth most human malignant disease and the third‐most common cause of cancer‐related death. Gambogic acid (GA) is a natural compound with a polyprenylated xanthone structure and possesses remarkable antitumor activity in a variety of cancer cells. However, the mechanism underlying the inhibitory effect of GA in GC is far from being completely understood. The goal of the present study is to investigate whether potential microRNAs are involved in antitumor effect of GA toward GC and to elucidate the possible mechanisms. We identified that miR‐26a‐5p was significantly increased by GA in GC cell lines and xenograft tumor. Downregulation of miR‐26a‐5p not only prevented GA‐induced inhibition on GC cell growth, but also suppressed GA‐induced apoptosis of GC cells. Informatics assay predicted that Wnt5a was regulated by miR‐26a‐5p and GA‐induced downregulation of Wnt5a was prevented by anti‐miR‐26a‐5p. Reporter gene assay showed that miR‐26a‐5p could negatively regulate Wnt5a through direct binding with 3ʹ‐UTR messenger RNA of Wnt5a. Thus, upregulation of Wnt5a exhibited the same action tendency for GA‐induced GC cell growth and apoptosis as observed by downregulation of miR‐26a‐5p. In conclusion, these results indicated that the inhibitory effect of GA on GC was mediated by the upregulation of miR‐26a‐5p and downregulation of Wnt5a. Our study provided new clues for the potential therapeutic effect of GA against GC and highlighted the importance of miR‐26a‐5p/Wnt5a pathway in the regulation of GC development.

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miR-26a-5p suppresses tumor metastasis by regulating EMT and is associated with prognosis in HCC

Abstract: Downregulation of miR-26a-5p promotes tumor metastasis by targeting EMT and influences the prognosis of HCC patients. Therefore, miR-26a-5p has potential as a new biomarker and therapeutic target.

Cited by 45 publications

References 43 publications

miR‑378a enhances the sensitivity of liver cancer to sorafenib by targeting VEGFR, PDGFRβ and c‑Raf

miR‑378a enhances the sensitivity of liver cancer to sorafenib by targeting VEGFR, PDGFRβ and c‑Raf

Dissimilar Appearances Are Deceptive–Common microRNAs and Therapeutic Strategies in Liver Cancer and Melanoma

Critical role of miR‐26a‐5p/Wnt5a signaling in gambogic acid‐induced inhibition of gastric cancer

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