MicroRNA-216a-3p promotes sorafenib sensitivity in hepatocellular carcinoma by downregulating MAPK14 expression

Zhong, Wu; Liu, Tingyu; Wang, Liang; Wang, Rong; Zhang, Hai

doi:10.18632/aging.103670

Cited by 7 publications

(4 citation statements)

References 37 publications

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“…ATF2 was shown to repress IFNβ1 transcription and to promote resistance to chemotherapy in melanoma [ 51 ]. Importantly, previous studies have found that ATF2 knockdown can increase the sensitivity of hepatocellular carcinoma cells to sorafenib [ [52] , [53] , [54] ], but the underlying mechanism has remained elusive. Consistently, our data revealed that ATF2 inhibition markedly promoted sorafenib-induced ferroptosis, which in turn enhanced the anticancer effects of sorafenib on GC cells in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

Increased ATF2 expression predicts poor prognosis and inhibits sorafenib-induced ferroptosis in gastric cancer

et al. 2023

Redox Biology

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Section: Discussionmentioning

confidence: 99%

Increased ATF2 expression predicts poor prognosis and inhibits sorafenib-induced ferroptosis in gastric cancer

et al. 2023

Redox Biology

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“…They incompletely or completely bind to the 3' untranslated region (3'-UTR) of target mRNAs, thus regulating cell signaling pathways through negatively mediating post-transcriptional gene expression or degrading mRNAs (17,18). Studies have shown that miR-216a-3p promotes cancer (19)(20)(21), and many reports showed that miR-216a-3p significantly influenced the activity of Wnt/β-catenin signaling pathway. Song et al (22).…”

Section: Introductionmentioning

confidence: 99%

miR‑216a‑3p inhibits osteogenic differentiation of human adipose‑derived stem cells via Wnt3a in the Wnt/β‑catenin signaling pathway

2022

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The current study aimed to investigate the potential function and mechanism of microRNA (miR)-216a-3p in the osteogenic differentiation of human adipose-derived stem cells (hADSCs). Dynamic expression changes of miR-216a-3p in the osteogenic differentiation of hADSCs were examined by reverse transcription-quantitative PCR (RT-qPCR). Regulatory effects of miR-216a-3p on the relative levels of osteogenesis-associated genes were also detected by RT-qPCR and western blotting. The relationship between miR-216a-3p and Wnt3a was verified through a dual-luciferase reporter assay. Furthermore, the influence of miR-216a-3p on the Wnt/β-catenin signaling pathway during the osteogenic differentiation of hADSCs was investigated by western blotting. The results revealed that during the osteogenic differentiation process of hADSCs, miR-216a-3p was downregulated and Wnt3a was upregulated. It was further verified that Wnt3a was the target of miR-216a-3p. Through inactivation of the Wnt/β-catenin signaling pathway, miR-216a-3p was able to mediate osteogenic differentiation of hADSCs. In conclusion, by targeting Wnt3a, miR-216a-3p mediated the osteogenic differentiation of hADSCs, which negatively regulated the Wnt/β-catenin signaling pathway.

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“…miR-631 targets PTPRE to dampen HCC migration, invasion, EMT, and intrahepatic metastasis [ 34 ]. Similar effects on liver cancer are also reflected in the other miRNAs like miR-199a-3p [ 35 ], miR-124-3p [ 36 ], and miR-216a-3p [ 37 ]. miR-373-3p is a novel miRNA first uncovered by Syring et al Its expression is substantially heightened in the serum of patients suffering from testicular germ cell tumors [ 38 ].…”

Section: Discussionmentioning

confidence: 83%

Upregulating microRNA-373-3p promotes apoptosis and inhibits metastasis of hepatocellular carcinoma cells

Wang

et al. 2022

Bioengineered

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Hepatocellular carcinoma (HCC) is one of the most prevalent malignancies in the digestive system. Abnormal miR-373-3p and TFAP4 expressions are critical in many malignant tumors, but it is unclear whether they work in the context of HCC. qRT-PCR measured miR-373-3p expression in HCC tissues and adjacent normal tissues. Flow cytometry and Western blot analyzed cell apoptosis. EMT, Transwell, and wound healing assay examined HCC cell migration and EMT, respectively. Western blot determined the profile of TFAP4/PI3K/AKT. IHC detected Ki67, E-cadherin, and vimentin in the tumor tissues. Moreover, the downstream target of miR-373-3p was predicted using the database. Dual luciferase activity assay and RIP verified the binding correlation between TFAP4 and miR-373-3p. In HCC tissues and cell lines, miR-373-3p was downregulated, and its overexpression stepped up HCC cell apoptosis and suppressed migration and EMT. Furthermore, miR-373-3p overexpression elevated Bax and caspase 3 expressions and attenuated Bcl2’s level. A xenograft tumor experiment in nude mice unveiled that miR-373-3p overexpression dampened tumor growth and proliferation. miR-373-3p cramped PI3K/AKT pathway activation. miR-373-3p negatively modulated TFAP4, and TFAP4 overexpression inverted miR-373-3p-mediated anti-tumor effects. Additionally, TFAP4 enhanced IGF1 expression, and promoted IGF1R-PI3K/AKT pathway activation. Collectively, miR-373-3p functions as an anti-tumor gene in HCC by inhibiting TFAP4/PI3K/AKT pathway.

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MicroRNA-216a-3p promotes sorafenib sensitivity in hepatocellular carcinoma by downregulating MAPK14 expression

Cited by 7 publications

References 37 publications

Increased ATF2 expression predicts poor prognosis and inhibits sorafenib-induced ferroptosis in gastric cancer

Increased ATF2 expression predicts poor prognosis and inhibits sorafenib-induced ferroptosis in gastric cancer

miR‑216a‑3p inhibits osteogenic differentiation of human adipose‑derived stem cells via Wnt3a in the Wnt/β‑catenin signaling pathway

Upregulating microRNA-373-3p promotes apoptosis and inhibits metastasis of hepatocellular carcinoma cells

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