Talin1 promotes HCC progression by regulating NRG1/PI3K/AKT axis

Abstract Hepatocellular carcinoma (HCC) is the world's third leading cause of cancer death, with metastasis being the predominant cause of treatment failure. We aim to explore the role of Talin1 in HCC and its underlying mechanism. We conducted bioinformatic analysis, qRT-PCR, Immunohistochemical staining, and western blot to detect the mRNA and protein expression levels of Talin1 in HCC tissues and adjacent samples from databases and our clinical center. Cell viability assays (CCK8 assay), transwell assays, and Xenograft tumor models were used to assess the effect of Talin1 on HCC cell proliferation, invasion, and migration both in vitro and in vivo. We also investigated the NRG1 protein, which is known to activate the PI3K/AKT pathway, to further elucidate the mechanism. Our results indicate that Talin1 is substantially more expressed in HCC tissues than in tumor-adjacent tissues in terms of both mRNA and protein levels. High expression levels of Talin1 were linked to poorer prognosis in HCC patients. Downregulation of Talin1 inhibited HCC cell proliferation and metastasis both in vitro and in vivo. Further, we found that Talin1 regulates NRG1, which activates the downstream PI3K/AKT pathway to facilitate HCC progression. Our findings suggest that Talin1 is an oncogene that regulates NRG1/ PI3K/AKT pathway to promote HCC progression. These findings provide new insight into HCC development and may offer novel treatment strategies for HCC.