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<p>Higd-1a is under expressed in colorectal cancer cells and its overexpression impaires the proliferation, migration, and invasiveness of colorectal cancer cells. However, the mechanism and clinical potential of Higd-1a in colorectal cancer remains to be further studied. This study investigated the potential of antitumor mechanism and clinical potential of Higd-1a in progression in colorectal cancer. We found that overexpression of Higd-1a in HCT-8 cancer cells suppressed tumor growth in nude mice. Higd-1a overexpression induced cle-caspase-3 and cle-caspase-9 and reduced Bcl-2 expressions, while p-AKT, p-JAK2 and p-STAT3 levels were significantly increased after downregulating Higd-1a in HCT-8 cancer cells. Ruxolitinib co-treatment completely enhanced the anticancer effect induced by inhibiting JAK2/AKT/STAT3 pathway in HCT-8 cells that downregulated Higd-1a. The expression rate in high Higd-1a expression group in stage I–II was considerably greater than that in stage III–IV, and Higd-1a expression and TNM stage were independent factors affecting the survival time of colorectal cancer. Higd-1a overexpression suppressed tumor growth in vivo and the molecular mechanisms may relate activation of apoptosis-related proteins and suppression JAK2/AKT/STAT3 pathway, and Higd-1a expression is helpful to evaluate the prognosis of colorectal cancer.</p>

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The potential antitumor mechanism and clinical potential of Higd-1a in colorectal cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月30日

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  • Zhenyu Xu,
  • Hanyue Zhang,
  • Yang Chen,
  • Yong Mao

摘要

Higd-1a is under expressed in colorectal cancer cells and its overexpression impaires the proliferation, migration, and invasiveness of colorectal cancer cells. However, the mechanism and clinical potential of Higd-1a in colorectal cancer remains to be further studied. This study investigated the potential of antitumor mechanism and clinical potential of Higd-1a in progression in colorectal cancer. We found that overexpression of Higd-1a in HCT-8 cancer cells suppressed tumor growth in nude mice. Higd-1a overexpression induced cle-caspase-3 and cle-caspase-9 and reduced Bcl-2 expressions, while p-AKT, p-JAK2 and p-STAT3 levels were significantly increased after downregulating Higd-1a in HCT-8 cancer cells. Ruxolitinib co-treatment completely enhanced the anticancer effect induced by inhibiting JAK2/AKT/STAT3 pathway in HCT-8 cells that downregulated Higd-1a. The expression rate in high Higd-1a expression group in stage I–II was considerably greater than that in stage III–IV, and Higd-1a expression and TNM stage were independent factors affecting the survival time of colorectal cancer. Higd-1a overexpression suppressed tumor growth in vivo and the molecular mechanisms may relate activation of apoptosis-related proteins and suppression JAK2/AKT/STAT3 pathway, and Higd-1a expression is helpful to evaluate the prognosis of colorectal cancer.