MiR-545-3p/MT1M axis regulates cell proliferation, invasion and migration in hepatocellular carcinoma

Liu, Changjun; Huang, Feizhou; Peng, Dezhen; Zhao, Liling; Mao, Xianhai

doi:10.1016/j.biopha.2018.09.009

Cited by 39 publications

(35 citation statements)

References 42 publications

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“…In breast cancer, miR-665 has been reported to inhibit B7-H3 expression 18. In HCC, miRNAs are also involved in cancer progression, such as cell proliferation, migration and invasion 19-22. Here, we also found that miR-665 was downregulated in HCC.…”

Section: Discussionsupporting

confidence: 58%

CircABCC2 Regulates Hepatocellular Cancer Progression by Decoying MiR-665

Bai¹,

Peng²,

Xia³

et al. 2019

J. Cancer

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Background : Numerous studies have shown that circular RNAs (circRNAs) play vital roles in tumor progression. However, how circRNAs function in hepatocellular cancer (HCC) remains mostly unclear. Methods : We analyzed HCC circRNA expression via a microarray, and the expression of an upregulated circRNA, circABCC2, was detected. We next explored the function of circABCC2 in HCC via a series of experiments. We performed RNA immunoprecipitation (RIP) and luciferase assays to explore the competing endogenous RNA (ceRNA) function of circABCC2 in HCC. Results : qRT-PCR verified that circABCC2 was overexpressed in HCC. Inhibition of circABCC2 suppressed HCC cell proliferation and invasion, but promoted apoptosis. Luciferase assays and RIP showed that circABCC2 and ABCC2 could directly bind to miR-665 and that circABCC2 could regulate ABCC2 expression by sponging miR-665. Conclusions : In summary, circABCC2 regulates ABCC2 expression and HCC progression by sponging miR-665. circABCC2 could be used as a biomarker and therapeutic target in HCC.

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Section: Discussionsupporting

confidence: 58%

CircABCC2 Regulates Hepatocellular Cancer Progression by Decoying MiR-665

Bai¹,

Peng²,

Xia³

et al. 2019

J. Cancer

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“…MiR-545-3p was an anti-cancer gene in multiple cancers. Chang et al proved that miR-545-3p inhibited the proliferation, migration and invasion of hepatocellular carcinoma cells via MT1M [28]. Song et al found that miR-545 hampered the growth of pancreatic ductal adenocarcinoma cells via RIG-1 [29].…”

Section: Discussionmentioning

confidence: 99%

Circ_0072083 interference enhances growth-inhibiting effects of cisplatin in non-small-cell lung cancer cells via miR-545-3p/CBLL1 axis

Liu

Qin

2020

Cancer Cell Int

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Background: Non-small-cell lung cancer (NSCLC) is one of the common cancers in the world. Circular RNA 0072083 (circ_0072083, circZFR) has been reported to be associated with the progression of NSCLC. In this study, we intended to explore the role and the potential mechanism of circ_0072083 in NSCLC. Methods: Quantitative real time polymerase chain reaction (qRT-PCR) was performed to detect the expression of circ_0072083, its matching linear RNA (zinc finger RNA binding protein (ZFR)) and microRNA-545-3p (miR-545-3p) in NSCLC cells. The ability of colony formation in NSCLC cells was detected by colony formation assay. The apoptosis and cell cycle were measured by flow cytometry. The metastasis was determined by transwell migration and invasion assays. The protein expression of E-cadherin, N-cadherin, Vimentin and Cbl proto-oncogene like 1 (CBLL1) was examined by western blot assay. The interaction between miR-545-3p and circ_0072083 or CBLL1 was predicted by starBase or Targetscan software. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were applied to validate these interactions. Nude mice bearing tumors were used to confirm the role of circ_0072083 and cisplatin (DDP) in vivo. Results: The level of circ_0072083 was higher in NSCLC tissues and cells relative to that in adjacent non-tumor tissues and normal lung cells. The transfection of si-circ_0072083 inhibited colony formation, cell cycle and metastasis while promoted the apoptosis of NSCLC cells stimulated by DDP. MiR-545-3p was a direct functional target of circ_0072083 in NSCLC cells. CBLL1 could bind to miR-545-3p in NSCLC cells. Circ_0072083 promoted the progression of NSCLC induced by DDP through sponging miR-545-3p and enhancing the enrichment of CBLL1 in vivo and in vitro. Conclusion: Circ_0072083 depletion contributed to DDP-triggered inhibition of NSCLC tumor through miR-545-3p/ CBLL1 axis.

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“…Hepatocellular carcinoma (HCC) is characterized by its high mortality rate, accompanied by chronic inflammatory reactions in liver 1. The step-by-step progression of HCC is characterized by alterations in the hepatic microenvironment 2.…”

Section: Introductionmentioning

confidence: 99%

<p>SIRT1 inhibits hepatocellular carcinoma metastasis by promoting M1 macrophage polarization via NF-κB pathway</p>

Zhou¹,

Yang²,

Li³

2019

OTT

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Background Tumor-associated macrophages (TAMs) serve as crucial modulators of the complicated interaction between cancer cells and immune microenvironment. Sirtuin 1 (SIRT1) has an impact on immune reactions in cancer progression. Current knowledge of the role of SIRT1 in the regulation of M1-like macrophages as well as in hepatocellular carcinoma (HCC) is insufficient. Methods SIRT1 expression in HCC tissues was detected using quantitative reverse transcriptase PCR (qRT-PCR) and Western blot. M1 markers were detected by qRT-PCR and flow cytometry assay. Moreover, the influence of SIRT1 on HCC cell apoptosis, migration, and invasion was studied using transwell assay, flow cytometry assay, and TUNEL assays, respectively. Results In this study, it was revealed that SIRT1 was upregulated in patients suffering from HCC; these patients were also shown to have elevated levels of M1-like TAM infiltration. SIRT1 was able to reinforce M1-like macrophage infiltration and inhibit HCC metastasis. Furthermore, SIRT1 enhanced NF-κB stimulation, promoting phosphorylation of p65, IκB, and IκB kinase. It was further demonstrated in our study that SIRT1 had an impact on polarization of M1 through the NF-κB pathway. NF-κB repression downregulated M1 markers in macrophages, which excessively expressed SIRT1 and counteracted the influence of SIRT1 on migration of HCC cells. Conclusion Taken together, these results offer proof that SIRT1 is an essential regulator of the immune reaction that counteracts malignant HCC cell migration as well as growth, indicating that macrophage SIRT1 could serve as an innovative target to treat HCC.

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MiR-545-3p/MT1M axis regulates cell proliferation, invasion and migration in hepatocellular carcinoma

Cited by 39 publications

References 42 publications

CircABCC2 Regulates Hepatocellular Cancer Progression by Decoying MiR-665

CircABCC2 Regulates Hepatocellular Cancer Progression by Decoying MiR-665

Circ_0072083 interference enhances growth-inhibiting effects of cisplatin in non-small-cell lung cancer cells via miR-545-3p/CBLL1 axis

<p>SIRT1 inhibits hepatocellular carcinoma metastasis by promoting M1 macrophage polarization via NF-κB pathway</p>

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MiR-545-3p/MT1M axis regulates cell proliferation, invasion and migration in hepatocellular carcinoma

Cited by 39 publications

References 42 publications

CircABCC2 Regulates Hepatocellular Cancer Progression by Decoying MiR-665

CircABCC2 Regulates Hepatocellular Cancer Progression by Decoying MiR-665

Circ_0072083 interference enhances growth-inhibiting effects of cisplatin in non-small-cell lung cancer cells via miR-545-3p/CBLL1 axis

<p>SIRT1 inhibits hepatocellular carcinoma metastasis by promoting M1 macrophage polarization via NF-&kappa;B pathway</p>

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<p>SIRT1 inhibits hepatocellular carcinoma metastasis by promoting M1 macrophage polarization via NF-κB pathway</p>