FOXG1 Enhances Paclitaxel Resistance in Prostate Cancer via NANOG-Mediated Cellular Stemness
Abstract
Background Paclitaxel (PTX) is an effective chemotherapeutic agent for prostate cancer (PCa), yet resistance emerges with disease progression. Cancer-cell stemness is intimately linked to PTX resistance. This work clarifies whether FOXG1 modulates PTX resistance in PCa via cellular stemness. Methods TCGA database was interrogated for FOXG1 expression in PCa. PTX-resistant PCa cell lines were generated by stepwise escalation of PTX concentration. qRT-PCR quantified FOXG1 and NANOG levels in PCa cells. CCK-8, sphere-formation assay, and flow cytometry evaluated cell viability, stemness, and apoptosis, respectively. Western blot assessed apoptosis-related proteins. JASPAR predicted FOXG1 binding sites within NANOG. Dual-luciferase reporter and ChIP verified FOXG1–NANOG interaction. Results Bioinformatic analysis revealed elevated FOXG1 expression in PCa tissues. FOXG1 levels were likewise increased in PCa cells. A PTX-resistant PC-3 sub-line (PC-3-R) was established. FOXG1 silencing suppressed stemness and viability of PC-3-R cells under PTX exposure while promoting apoptosis. FOXG1 was identified as an upstream regulator of NANOG. NANOG overexpression reversed the effects conferred by FOXG1 silencing on PC-3-R cells. Conclusion FOXG1 fosters NANOG-mediated cellular stemness to potentiate PTX resistance in PCa.
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BibTeX
@article{shen2026foxg1,
title = {{FOXG1 Enhances Paclitaxel Resistance in Prostate Cancer via NANOG-Mediated Cellular Stemness}},
author = {Chong Shen and Yu Ren and Xiangrong Ying and Gangfeng Wu and Chuanchuan Zhan and Zhengang Luo and Shuixiang Tao and Haojie Zhang},
journal = {American Journal of Men's Health},
year = {2026},
month = oct,
doi = {10.1177/15579883261500924},
url = {https://doi.org/10.1177/15579883261500924},
note = {CC BY},
}
RIS
TY - JOUR
TI - FOXG1 Enhances Paclitaxel Resistance in Prostate Cancer via NANOG-Mediated Cellular Stemness
AU - Chong Shen
AU - Yu Ren
AU - Xiangrong Ying
AU - Gangfeng Wu
AU - Chuanchuan Zhan
AU - Zhengang Luo
AU - Shuixiang Tao
AU - Haojie Zhang
PY - 2026
DA - 2026/10/23
JO - American Journal of Men's Health
DO - 10.1177/15579883261500924
UR - https://doi.org/10.1177/15579883261500924
AB - Background Paclitaxel (PTX) is an effective chemotherapeutic agent for prostate cancer (PCa), yet resistance emerges with disease progression. Cancer-cell stemness is intimately linked to PTX resistance. This work clarifies whether FOXG1 modulates PTX resistance in PCa via cellular stemness. Methods TCGA database was interrogated for FOXG1 expression in PCa. PTX-resistant PCa cell lines were generated by stepwise escalation of PTX concentration. qRT-PCR quantified FOXG1 and NANOG levels in PCa cells. CCK-8, sphere-formation assay, and flow cytometry evaluated cell viability, stemness, and apoptosis, respectively. Western blot assessed apoptosis-related proteins. JASPAR predicted FOXG1 binding sites within NANOG. Dual-luciferase reporter and ChIP verified FOXG1–NANOG interaction. Results Bioinformatic analysis revealed elevated FOXG1 expression in PCa tissues. FOXG1 levels were likewise increased in PCa cells. A PTX-resistant PC-3 sub-line (PC-3-R) was established. FOXG1 silencing suppressed stemness and viability of PC-3-R cells under PTX exposure while promoting apoptosis. FOXG1 was identified as an upstream regulator of NANOG. NANOG overexpression reversed the effects conferred by FOXG1 silencing on PC-3-R cells. Conclusion FOXG1 fosters NANOG-mediated cellular stemness to potentiate PTX resistance in PCa.
SN - 1557-9891
SN - 1557-9883
ER -