Deciphering the molecular interplay and tumorigenesis in hepatocellular carcinoma through insights into FBXL6 and KRAS^(G12D)  

作　　者：Qiang Cai Quazi T.H.Shubhra 

机构地区：[1]Department of Neurosurgery,Renmin Hospital of Wuhan University,Wuhan 430060,China [2]Institute of Chemistry,University of Silesia in Katowice,41‑500 Chorzow,Poland

出　　处：《Military Medical Research》2025年第3期464-466,共3页军事医学研究(英文版)

基　　金：supported by the National Natural Science Foundation of China(82271518,81971158,and 81671306);the Interdisciplinary Innovative Talents Foundation from Renmin Hospital of Wuhan University(JCRCFZ-2022-030);the Guiding Projects of Traditional Chinese Medicine in 2023–2024 by Hubei Provincial Administration of Traditional Chinese Medicine(ZY2023F038).

摘　　要：Liver cancer,particularly hepatocellular carcinoma,remains a formidable challenge in medical research and requires a deeper understanding of its molecular underpinnings.In a fascinating recent study published in Military Medical Research,Xiong et al.[1]revealed the complex roles of F-box and leucine-rich repeat 6(FBXL6)and Kirsten rat sarcoma(KRAS)^(G12D) in the pathogenesis of liver cancer.This research offers critical insights into how these proteins contribute to hepatocellular carcinoma development and progression,potentially paving the way for targeted therapeutic strategies.This commentary analyzes the key findings from this study and their broader implications in oncology.

关 键 词：Hepatocellular carcinoma F-box and leucine-rich repeat 6(FBXL6)activation Kirsten rat sarcoma(KRAS)^(G12D)mutation Mitogen-activated protein kinase(MEK)/mammalian target of rapamycin(mTOR)pathway Metastasis 

分 类 号：R735.7[医药卫生—肿瘤]