Background <p>Vitamin K2 has been reported to inhibit proliferation in several cancer types, including hepatocellular carcinoma (HCC), while albumin serves as a prognostic indicator in HCC and has also been shown to suppress HCC cell growth in vitro. Despite these observations, the effect of combined Vitamin K2 and albumin exposure on HCC cell fate has not been systematically examined.</p> Methods and Results <p>We compared the effects of Vitamin K2, albumin, and their combined exposure across multiple HCC cell lines, assessing viability, proliferative capacity, and selected regulatory markers to evaluate growth- and fate-associated responses. Combined exposure consistently produced stronger suppression of proliferation and colony formation than either treatment alone. These effects were accompanied by cell-cycle arrest, reduced AFP expression, and impaired wound-healing capacity. Importantly, combined treatment altered cell death patterns by reducing necrosis and favoring apoptotic progression, whereas senescence-associated responses were limited and cell-line-dependent.</p> Conclusions <p>These findings indicate that concurrent Vitamin K2 and albumin exposure modulates proliferation and cell fate decisions in HCC cells and underscore the value of evaluating combinatorial effects through integrated phenotypic outcomes.</p>

错误:搜索内容不能为空,请输入英文关键词
错误:关键词超出字数限制,请精简
高级检索

Combined treatment with vitamin K2 and albumin inhibits growth in hepatocellular carcinoma cells by promoting differentiation and apoptosis

  • Helin Sagir,
  • Tugce Batur,
  • Brian I. Carr,
  • Hani Alotaibi

摘要

Background

Vitamin K2 has been reported to inhibit proliferation in several cancer types, including hepatocellular carcinoma (HCC), while albumin serves as a prognostic indicator in HCC and has also been shown to suppress HCC cell growth in vitro. Despite these observations, the effect of combined Vitamin K2 and albumin exposure on HCC cell fate has not been systematically examined.

Methods and Results

We compared the effects of Vitamin K2, albumin, and their combined exposure across multiple HCC cell lines, assessing viability, proliferative capacity, and selected regulatory markers to evaluate growth- and fate-associated responses. Combined exposure consistently produced stronger suppression of proliferation and colony formation than either treatment alone. These effects were accompanied by cell-cycle arrest, reduced AFP expression, and impaired wound-healing capacity. Importantly, combined treatment altered cell death patterns by reducing necrosis and favoring apoptotic progression, whereas senescence-associated responses were limited and cell-line-dependent.

Conclusions

These findings indicate that concurrent Vitamin K2 and albumin exposure modulates proliferation and cell fate decisions in HCC cells and underscore the value of evaluating combinatorial effects through integrated phenotypic outcomes.