SLC41A3 (Solute Carrier Family 41 Member 3)

Conversely, the high-risk group exhibited distinct genomic features and was predicted to be more sensitive to specific targeted agents, including Navitoclax and Sorafenib. We identified and validated a novel 7-gene prognostic signature derived from a subpopulation of EGFR-TKI-resistant macrophages. This signature accurately predicts patient survival, offers insights into the molecular mechanisms of therapy resistance in HCC, and provides a promising tool for improved patient stratification and the development of personalized treatment strategies.

Rare variant analysis identified a deleterious frameshift deletion in SLC41A3 as a risk factor for sarcopenia. Our findings suggest that the suppression of MYOG could play a role in myogenesis or muscle maintenance, although this mutation did not impact the terminal differentiation of human myoblasts. Additionally, HLA analysis revealed that HLA-DPB1*02:01 has a protective effect, especially in Northeast Asian populations. Our study enhances the understanding of the etiology of sarcopenia and provides new insights into the mechanisms of its pathogenesis.

Cellular experiments showed that knockdown of SLC41A1 inhibited proliferation, migration and invasion of HCC, whereas SLC41A1 overexpression exerted the tumor-promoting effects. Collectively, our results shed light on new insights into expression, putative roles and mechanisms of SLC41A1 in HCC, providing novel diagnostic biomarkers and therapeutic targets for HCC.

The 7-SLC-gene prognostic signature established in this study helped predict the prognosis, and was also correlated with the tumor immune status and infiltration of different immune cells in the tumor microenvironment. The current findings may provide important clinical indications for proposing a novel combination therapy consists of targeted anti-SLC therapy and immunotherapy for HCC patients.