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Last update 08 May 2025

MIR7-3HG

Last update 08 May 2025

Basic Info

Synonyms

C19orf30, Huh7, LINC00306

+ [9]

Introduction-

Drugs associated with MIR7-3HG

CN116082460

Patent Mining

Target

MIR7-3HG

Mechanism-

Active Org.

Fudan University

Originator Org.

Fudan University

Active Indication

Liver Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

CN116332940

Patent Mining

Target

MIR7-3HG

Mechanism-

Active Org.

Guangxi Minzu University

Originator Org.

Guangxi Minzu University

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MIR7-3HG

100 Translational Medicine associated with MIR7-3HG

0 Patents (Medical) associated with MIR7-3HG

2,116

Literatures (Medical) associated with MIR7-3HG

01 Dec 2025·Immunologic Research

HBx/WDR5 enhances IGF-1 transcription in hepatocellular carcinoma cells and promotes recruitment, infiltration, and activity of Treg cells

Article

Author: Jia, Yi ; Wang, Erli ; Bai, Zhe ; Sun, Shuhua ; Li, Hui

HBV X protein (HBx), the smallest open reading frame in the hepatitis B virus (HBV) genome, can promote hepatocellular carcinoma (HCC) tumorigenesis by activating the expression of multiple oncogenes through inducing epigenetic alterations and interacting with the underlying transcriptional machinery. HBV non-infected HepG2 and Huh7 cells were transfected with HBx expression plasmids. The transcriptional, protein expression, and secretion levels of IGF-1 were detected by RT-qPCR, western blot, and ELISA, respectively. ChIP-qPCR was used to analyze the binding proteins on the IGF-1 gene. A co-culture system of HCC and Treg cells was designed using Transwell chambers. IGF-1 mRNA, protein, and secretion levels were increased in HepG2 and Huh7 cells exogenously expressing HBx. HBx was able to enter the nucleus and interact with the enhancer region of the IGF-1 gene. Levels of WDR5 and H3K4me1, which bind to the enhancer region of the IGF-1 gene, were also increased in HepG2 and Huh7 cells ectopically expressing HBx. Knockdown of WDR5 counteracted the upregulation of IGF-1 mRNA and protein levels by HBx. In the cell co-culture system, HBx/IGF-1 signaling in HCC cells promoted Treg cells expansion, IL-10 secretion, and infiltration, which was blocked by the IGF-1R inhibitor picropodophyllin. HBx/WDR5 promoted IGF-1 transcription in HCC cells through enhancers. HBx could promote Treg cell recruitment, infiltration, and activity by enhancing IGF-1 expression. IGF-1/IGF-1R signaling plays an important role in the communication between HCC cells and Treg cells. Targeting WDR or IGF-1/IGF-1R would be beneficial for the treatment of HCC.

01 Jul 2025·Cellular Signalling

GINS4 silencing mediates hepatocellular cancer cell proliferation, cycle and ferroptosis through POLE2

Article

Author: Wang, Congyu ; Song, Rui ; Xu, Zhe ; Yao, Jinni ; Yang, Huaicheng ; Zeng, Xiangrui ; Zhang, Zheng ; Yuan, Meng ; Liao, Heqiang

BACKGROUNDGINS4 has been identified as a regulator associated with multiple types of cancers. However, the effects of GINS4 on hepatocellular carcinoma (HCC) have not been reported.METHODSGINS4 expression in HCC was evaluated utilizing UALCAN database. The relationship between the expression of GINS4 and the survival probability of HCC patients was analyzed using Kaplan-Meier Plotter. Cell viability was evaluated by CCK8 assay and EDU assay. qRT-PCR and western blot were performed to examine GINS4 expression. The level of cell cycle was measured by flow cytometry and western blot. Fe²⁺ level and ferroptosis-related proteins were measured by corresponding kits and western blot. Lipid peroxidation was explored by C11 BODIPY 581/591 probe. STRING database and HDOCK database were performed to predict the binding of GINS4 to POLE2. Immunofluorescence and western blotting was adopted for assessing cell autophagy and mTOR signaling pathway. Ki67 and GPX4 levels were measured by immunohistochemistry. The expression levels of POLE2/PI3K/AKT were assessed by western blot.RESULTSThe data indicated that GINS4 expression was upregulated in HCC. Knockdown of GINS4 alleviated the proliferation and cycle and promoted ferroptosis of HuH7 cells. GINS4 was proved to bind to POLE2 and the silencing of GINS4 inhibited the expression of POLE2. GINS4 knockdown accelerated ferroptosis in HuH7 cells. POLE2 overexpression reversed the influences of GINS4 silencing on proliferation and cycle, and also ferroptosis. In addition, interference with GINS4 suppressed the activation of PI3K/AKT signaling via POLE2. In vivo experiments illustrated that GINS4 deletion suppressed HCC tumor growth, increased the GPX4 expression and restrained the Ki67 level, as well as reducing POLE2/PI3K/AKT signaling.CONCLUSIONGINS4 silencing suppressed proliferation and cycle while promoted ferroptosis in HCC cells by regulating PI3K/AKT signaling via binding to POLE2.

01 Jul 2025·Journal of Hazardous Materials

Diesel exhaust promoted diethylnitrosamine-induced hepatocarcinogenesis in mice

Article

Author: Ma, Yuanyuan ; Wu, Dong ; Luan, Qi ; Chen, Sixin ; Chen, Yixin ; Xiao, Hua ; Han, Wei ; Cui, Lianhua ; Dou, Junjie ; Zhang, Shuxin ; Cai, Zhengguo

Exposure to diesel exhaust (DE) has been linked to an increased risk of various cancers, including liver cancer. However, the underlying mechanisms driving this association remain insufficiently understood. In this study, we employed a diethylnitrosamine (DEN)-induced mouse liver tumor model and conducted a 19-week combined exposure (750 μg/m³) using a DE exposure system. Our results demonstrated that long-term DE exposure activates cancer-related genes and enhances the formation of DEN-induced liver tumors. Compared to the DEN group, mice in the DEN + diesel exhaust exposure (DEE) group exhibited lower body weight, higher tumor formation rates and more severe DNA damage. The tumor-promoting effect of DE may be associated with the upregulation of SEMA4D and the activation of the PI3K/AKT signaling pathway. Additionally, liver cells in the DEE group exhibited nuclear atypia, a characteristic feature of cancerous transformation. In vitro studies have revealed that exposure to diesel exhaust particles (DEP) promotes the proliferation of HepG2 cells and HUH7 cells by upregulating SEMA4D and activating the PI3K/AKT signaling pathway. This effect was attenuated by inhibiting either SEMA4D or PI3K. This study was the first to identify that DE exposure promotes the development of DEN-induced liver tumors in mice, with the mechanism potentially involving the SEMA4D/PI3K/AKT pathway. These findings provide novel insights into the hepatotoxic effects of DE and highlight the need for further investigation into its carcinogenic potential.

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MIR7-3HG

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