Journal: Apoptosis
Article Title: Hypoxic glycolysis-driven histone lactylation activates NHE7 to promote endometrial cancer progression via COX6C-mediated endoplasmic reticulum stress
doi: 10.1007/s10495-026-02262-w
Figure Lengend Snippet: NHE7 facilitates EC tumor growth by upregulating COX6C expression in vivo. A WB analysis was used to detect the protein expression levels of NHE7 and COX6C in Ishikawa cells overexpressing NHE7, and in Ishikawa cells with concurrent NHE7 overexpression and COX6C knockdown. B Stable Ishikawa cell lines were established for the following conditions: NHE7 overexpression alone, and concurrent NHE7 overexpression with COX6C knockdown, along with their respective control cells. A xenograft tumor model was then generated using these cells. C Tumor growth was monitored and recorded, and D tumor weight was measured at the endpoint. E WB assay was performed to assess the effects of NHE7 overexpression alone or in combination with COX6C knockdown on the levels of apoptosis markers c-PARP and C-Caspase3 in xenograft tumor tissues. F HE staining was performed to assess histopathological damage in xenograft tumor tissues following NHE7 overexpression, either alone or in combination with COX6C knockdown. IHC was performed to evaluate the impact of NHE7 overexpression, either alone or in combination with COX6C knockdown, on the expression of Ki67, E-cadherin, N-cadherin, Vimentin, OCT4, Nanog, SOX2, p-IRE1α, IRE1α, and ATF6 in xenograft tumor tissues. Scale bar, 50 μm (400 ×) and 100 μm (200 ×). At least three independent experiments were performed on the assays. Error bars represent the mean ± SD ( n = 3). * P < 0.05,** P < 0.01
Article Snippet: p-IRE1α , BIOSS , bs-16698R , WB/IHC.
Techniques: Expressing, In Vivo, Over Expression, Knockdown, Control, Generated, Staining