Additional file 1 of Mitochondrial HMGCS1 mediates cisplatin resistance in cervical cancer through regulation of mitochondrial transcription

Supplementary Material 1: Supplementary Fig. S1. HMGCS1 status and subcellular localization do not affect the basal proliferation of cervical cancer cells. (A-B) Proliferation curves of wild-type (WT) and HMGCS1 knockout (KO) HeLa (A) and C33A (B) cells. (C-D) Western blot analysis confirming comparable expression levels of 6xHis-tagged constructs in total cell lysates of HeLa (C) and C33A (D) cells expressing empty vector (EV), mitochondria-targeted HMGCS1 (MTS), or nuclear-localized HMGCS1 (NLS). TUBA1A serves as a loading control. (E) Western blot analysis of subcellular fractions (nuclei, cytosol, mitochondria) from HeLa cells expressing the constructs. The 6xHis tag confirms the specific localization of NLS-HMGCS1 to the nucleus and MTS-HMGCS1 to the mitochondria, with minimal cytosolic mislocalization. Lamin B1, TUBA1A, and Tomm20 serve as markers for nuclear, cytosolic, and mitochondrial fractions, respectively. (F-I) Proliferation curves of wild-type (F, G) and HMGCS1-KO (H, I) cells expressing EV, MTS, or NLS constructs. Cell proliferation was measured over a 5-day period using the SRB assay. Data for proliferation curves are presented as mean ± SD. ns: not significant, by Two-way ANOVA