Overexpression of ZFP69B promotes hepatocellular carcinoma growth by upregulating the expression of TLX1 and TRAPPC9.

Background: T-cell leukemia homeobox protein 1 (TLX1) has been revealed as a hub transcription factor in leukemia, while its function in hepatocellular carcinoma (HCC) has not been well described. Here, we investigated the regulation and function of TLX1 in HCC.

Methods: TLX1 and its possible upstream and downstream molecules in HCC were identified using bioinformatics tools, which were then verified by RT-qPCR assay.

MTFR2 accelerates hepatocellular carcinoma mediated by metabolic reprogramming via the Akt signaling pathway.

Metabolic reprogramming has recently been identified as a hallmark of malignancies. The shift from oxidative phosphorylation to glycolysis in hepatocellular carcinoma (HCC) meets the demands of rapid cell growth and provides a microenvironment for tumor progression. This study sought to uncover the function and mechanism of MTFR2 in the metabolic reprogramming of HCC.

Activating transcription factor 2 promotes the progression of hepatocellular carcinoma by inducing the activation of the WHSC1-mediated TOP2A/PI3K/AKT axis.

Activating transcription factor 2 (ATF2) is a tumor driver gene implicated in several human malignancies. This study aimed to determine the roles of ATF2 and its related molecules in the tumorigenesis of hepatocellular carcinoma (HCC). According to the Pan-cancer bioinformatics system, ATF2 is highly expressed in HCC.

Lysine demethylase 5C epigenetically reduces transcription of ITIH1 that results in augmented progression of liver hepatocellular carcinoma.

Lysine demethylase 5C (KDM5C) is a member of the KDM family of demethylases and has been reported as a cancer driver. This study aimed to probe the function of KDM5C in the development of liver hepatocellular carcinoma (LIHC) and the molecules of action. According to data from publicly accessible bioinformatic databases, KDM5C is highly expressed in LIHC and associated with poor patient prognosis.

ETV4 transcriptionally activates HES1 and promotes Stat3 phosphorylation to promote malignant behaviors of colon adenocarcinoma.

Colon adenocarcinoma (COAD) is the commonest type of colorectal cancer with high morbidity and mortality worldwide. ETS variant 4 (ETV4) is a member of the ETS transcription factors and is frequently involved in the progression of many cancers. This study focused on the relevance of ETV4 to the progression of COAD.