<i>MiR-331-3p</i> Inhibition of the Hepatocellular Carcinoma (HCC) Bel-7402 Cell Line by Down-Regulation of E2F1

Jin, Wenjian; Zhong, Ning; Wang, Lingling; Yu, Jieli; Yin, Fugen; Zhang, Kun‐He

doi:10.1166/jnn.2019.16535

Cited by 20 publications

(15 citation statements)

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“…(An et al 2015) E2F1 is a transcription factor that has been known to promote HCC progression. (Farra et al 2017) Besides the findings in this study, miR-331-3p (Jin et al 2019) and miR-34a (Han et al 2019) have also been found to regulate E2F1 expression in HCC cell lines. However, precise interactions between E2F1 and miRNAs need further exploration.…”

Section: Discussionsupporting

confidence: 73%

Peer Review #1 of "Identification of key genes and long non-coding RNA associated ceRNA networks in hepatocellular carcinoma (v0.2)"

2019

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Background. Hepatocellular carcinoma (HCC) is one of the leading causes of cancerrelated deaths worldwide. Although multiple efforts have been made to understand the development of HCC, morbidity and mortality rates remain high. In this study, we aimed to discover the mRNAs and long non-coding RNAs (lncRNAs) that contribute to the progression of HCC. We constructed a lncRNA-related competitive endogenous RNA (ceRNA) network to elucidate the molecular regulatory mechanism underlying HCC. Methods. A microarray dataset (GSE54238) containing information about both mRNAs and lncRNAs was downloaded from the GEO database. Differentially expressed genes (DEGs) and lncRNAs (DElncRNAs) in tumor tissues and non-cancerous tissues were identified using the limma package of the R software. The miRNAs that are targeted by DElncRNAs were predicted using miRcode, while the target mRNAs of miRNAs were retrieved from miRDB, miRTarBas, and TargetScan. Functional annotation and pathway enrichment of DEGs were performed using the EnrichNet website. We constructed a protein-protein interaction (PPI) network of DEGs using STRING, and identified the hub genes using Cytoscape. Survival analysis of the hub genes and DElncRNAs was performed using the GEPIA database. The expression of molecules with prognostic values was validated on the UALCAN database. The hepatic expression of hub genes was examined using The Human Protein Atlas. The hub genes and DElncRNAs with prognostic values as well as the predictive miRNAs were selected to construct the ceRNA networks. Results. We found that 10 hub genes (KPNA2, MCM7, CKS2, KIF23, HMGB2, ZWINT, E2F1, MCM4, H2AFX, and EZH2) and four lncRNAs (FAM182B, SNHG6, SNHG1, and SNHG3) with prognostic values were overexpressed in the hepatic tumor samples. We also constructed a network containing 10 lncRNA-miRNA-mRNA pathways, which might be responsible for

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Section: Discussionsupporting

confidence: 73%

Peer Review #1 of "Identification of key genes and long non-coding RNA associated ceRNA networks in hepatocellular carcinoma (v0.2)"

2019

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“…Previous studies characterized the miRNA expression profiles related with growth and metastasis and prognosis of HCC, and dysregulation of miRNAs plays a vital role in hepatic carcinogenesis 17,18. miRNAs could act as potential biomarkers in HCC 19.…”

Section: Discussionmentioning

confidence: 99%

<p>MicroRNA-3651 promotes the growth and invasion of hepatocellular carcinoma cells by targeting PTEN</p>

Zhao

Song

Miao

et al. 2019

OTT

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BackgroundHepatocellular carcinoma (HCC) is one of the most common malignant tumors in human worldwide. Evidence indicated that upregulation of microRNA-3651 (miR-3651) was observed in human HCC tissues. In this study, we explored the mechanisms by which miR-3651 regulated the proliferation, apoptosis and invasion of HCC.MethodsThe levels of miR-3651 in human HCC tissues were detected using qRT-PCR assay. In addition, transwell invasion and Western blot assay were conducted to detect cell invasion and apoptosis, respectively. Meanwhile, the dual-luciferase reporter assay was used to explore the interaction of miR-3651 and phosphate and tension homology deleted on chromsome ten (PTEN) in HCC.ResultsThe levels of miR-3651 were upregulated in HCC tissues in comparison with the matched normal tissues. Overexpression of miR-3651 significantly promoted the proliferation and invasion of Huh-7 cells. In contrast, inhibition of miR-3651 markedly inhibited the proliferation and invasion of Huh-7 cells via promoting apoptosis. Moreover, downregulation of miR-3651 markedly inhibited tumor growth in vivo. Furthermore, bioinformatics analysis and luciferase reporter assay identified that PTEN was the directly binding target of miR-3651 in Huh-7 cells. Meanwhile, overexpression of miR-3651 obviously decreased the level of PTEN, and increased the expressions of p-p85 and p-Akt in Huh-7 cells.ConclusionThese results indicated that miR-3651 might act as a potential oncogene in HCC by targeting PTEN. Therefore, miR-3651 might be a novel therapeutic target for the treatment of HCC.

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“… 11 Studies have also shown that miR-331-3p is involved in tumor proliferation, apoptosis, metastasis, and epithelial-to-mesenchymal transition (EMT). 8 - 10 , 12 As cell apoptosis and EMT are closely associated with drug resistance, we inferred that miR-331-3p may also participate in drug resistance. Our previous studies have demonstrated that miR-331-3p is upregulated in PC and promotes PC cell proliferation and EMT-mediated metastasis by targeting ST7L.…”

Section: Introductionmentioning

confidence: 96%

“… 6 Recently, several miRNAs have been found to play important roles in tumor drug resistance via the regulation of oncogenes or tumor suppressor genes. 7 It has been shown that miR-331-3p plays an important role in many tumors, such as colorectal cancer, 8 liver cancer, 9 lung cancer, 10 and gastric cancer. 11 Studies have also shown that miR-331-3p is involved in tumor proliferation, apoptosis, metastasis, and epithelial-to-mesenchymal transition (EMT).…”

Section: Introductionmentioning

confidence: 99%

MiR-331-3p Links to Drug Resistance of Pancreatic Cancer Cells by Activating WNT/β-Catenin Signal via ST7L

Zhan

Chen

Xia

et al. 2020

Technol Cancer Res Treat

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Background: Pancreatic cancer is an aggressive type of cancer with poor prognosis, short survival rate, and high mortality. Drug resistance is a major cause of treatment failure in the disease. MiR-331-3p has been reported to play an important role in several cancers. We previously showed that miR-331-3p is upregulated in pancreatic cancer and promotes pancreatic cancer cell proliferation and epithelial-to-mesenchymal transition–mediated metastasis by targeting ST7L. However, it is uncertain whether miR-331-3p is involved in drug resistance. Methods: We investigated the relationship between miR-331-3p and pancreatic cancer drug resistance. As part of this, microRNA mimics or inhibitors were transfected into pancreatic cancer cells. Quantitative polymerase chain reaction was used to detect miR-331-3p expression, and flow cytometry was used to detect cell apoptosis. The Cell Counting Kit-8 assay was used to measure the IC50 values of gemcitabine in pancreatic cancer cells. The expression of multidrug resistance protein 1, multidrug resistance-related protein 1, breast cancer resistance protein, β-Catenin, c-Myc, Cyclin D1, Bcl-2, and Caspase-3 was evaluated by Western blotting. Results: We confirmed that miR-331-3p is upregulated in gemcitabine-treated pancreatic cancer cells and plasma from chemotherapy patients. We also confirmed that miR-331-3p inhibition decreased drug resistance by regulating cell apoptosis and multidrug resistance protein 1, multidrug resistance-related protein 1, and breast cancer resistance protein expression in pancreatic cancer cells, whereas miR-331-3p overexpression had the opposite effect. We further demonstrated that miR-331-3p effects in drug resistance were partially reversed by ST7L overexpression. In addition, overexpression of miR-331-3p activated Wnt/β-catenin signaling in pancreatic cancer cells, and ST7L overexpression restored activation of Wnt/β-catenin signaling. Conclusions: Taken together, our data demonstrate that miR-331-3p contributes to drug resistance by activating Wnt/β-catenin signaling via ST7L in pancreatic cancer cells. These data provide a theoretical basis for new targeted therapies in the future.

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MiR-331-3p Inhibition of the Hepatocellular Carcinoma (HCC) Bel-7402 Cell Line by Down-Regulation of E2F1

Cited by 20 publications

References 0 publications

Peer Review #1 of "Identification of key genes and long non-coding RNA associated ceRNA networks in hepatocellular carcinoma (v0.2)"

Peer Review #1 of "Identification of key genes and long non-coding RNA associated ceRNA networks in hepatocellular carcinoma (v0.2)"

<p>MicroRNA-3651 promotes the growth and invasion of hepatocellular carcinoma cells by targeting PTEN</p>

MiR-331-3p Links to Drug Resistance of Pancreatic Cancer Cells by Activating WNT/β-Catenin Signal via ST7L

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