Loss of exosomal miR-200b-3p from hypoxia cancer-associated fibroblasts promotes tumorigenesis and reduces sensitivity to 5-Flourouracil in colorectal cancer via upregulation of ZEB1 and E2F3

Gong, Wenjing; Guo, Yang; Yuan, Hang; Chai, Rui; Wan, Ziang; Zheng, Bo’an; Hu, Xinye; Chen, Bingchen; Gao, Shan; Dai, Qiaoqiong; Yu, Peng; Tu, Shiliang

doi:10.1038/s41417-023-00591-5

Cited by 5 publications

(1 citation statement)

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“…Moreover, 5‐Fluorouracil (5‐FU)‐based chemotherapy is extensively employed for advanced GC patients 4 . Unfortunately, as a result of multiple complex mechanisms such as DNA damage response and hypoxia, patients become increasingly resistant to 5‐FU and eventually relapse 5,6 . Thus, further elucidation of the underlying molecular mechanisms accounting for the aggressive characteristics of GC cells will contribute to discovering better strategies for both prevention and therapy for GC patients.…”

Section: Introductionmentioning

confidence: 99%

The FOXO1/G6PC axis promotes gastric cancer progression and mediates 5‐fluorouracil resistance by targeting the PI3K/AKT/mTOR signaling pathway

Han,

Liu,

et al. 2024

Molecular Carcinogenesis

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Gastric cancer (GC) is a prevalent malignancy of the digestive system. Distant metastasis and chemotherapy resistance are the crucial obstacles to prognosis in GC. Recent research has discovered that the glucose‐6‐phosphatase catalytic subunit (G6PC) plays an important role in tumor malignant development. However, little evidence has highlighted its role in GC. Herein, through a comprehensive analysis including profiling of tissue samples and functional validation in vivo and in vitro, we identify G6PC as a crucial factor in GC tumorigenesis. Importantly, we found that the FOXO1/G6PC axis could accelerate GC cell proliferation, metastasis, and 5‐Fluorouracil (5‐FU) resistance by targeting the PI3K/AKT/mTOR signaling pathway, implicating that as a prospective therapeutic approach in GC.

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Section: Introductionmentioning

confidence: 99%