EGR1//SOX5 轴调节膀胱癌细胞的迁移、侵袭和吉西他滨耐药性。
EGR1//SOX5 axis modulates migration, invasion and Gemcitabine resistance of bladder cancer cells.
机构信息
Basic Medical College, Jiamusi University, Jiamusi, Heilongjiang, China.
Department of Oncology Comprehensive Treatment, The First Affiliated Hospital of Jiamusi University, Jiamusi, Heilongjiang, China.
出版信息
Cancer Biol Ther. 2023 Dec 31;24(1):2270106. doi: 10.1080/15384047.2023.2270106. Epub 2023 Oct 20.
BACKGROUND
Bladder cancer is one of the most common malignant tumors of the urinary system, and its incidence is increasing worldwide. However, the underlying mechanisms that trigger migration, invasion and chemotherapy resistance are unclear.
RESULTS
Bioinformatics analysis of bladder cancer cohort indicated that is deregulated in bladder cancer. was validated and highly expressed in bladder cancer patients and cell lines. In addition, induced the migration, invasion and Gemcitabine resistance of bladder cancer cells. We identified that the transcription factor EGR1 directly repressed and thereby suppressed the migration and invasion of bladder cancer cells. Furthermore, interacted with miR-142, which subsequently regulated the expression of SOX5, a well-studied oncogene and targeted by miR-142. In addition, EGR1 served as a suppressive transcription factor of . Therefore, EGR1 directly or indirectly regulates SOX5 via /miR-142 axis. induced Gemcitabine resistance by promoting autophagy.
CONCLUSIONS
EGR1, /miR-142 and SOX5 form a coherent feed-forward loop that modulates the migration, invasion and Gemcitabine resistance of bladder cancer.
背景
膀胱癌是泌尿系统最常见的恶性肿瘤之一，其发病率在全球范围内呈上升趋势。然而，触发迁移、侵袭和化疗耐药的潜在机制尚不清楚。
结果
膀胱癌队列的生物信息学分析表明， 在膀胱癌中失调。 在膀胱癌患者和细胞系中得到验证和高表达。此外， 诱导膀胱癌细胞的迁移、侵袭和吉西他滨耐药。我们确定转录因子 EGR1 直接抑制 ，从而抑制膀胱癌细胞的迁移和侵袭。此外， 与 miR-142 相互作用，随后调节 miR-142 的靶基因 SOX5 的表达，SOX5 是一个研究充分的癌基因。此外，EGR1 是 的抑制性转录因子。因此，EGR1 通过 /miR-142 轴直接或间接调节 SOX5。 通过促进自噬诱导吉西他滨耐药。
结论
EGR1、/miR-142 和 SOX5 形成一个连贯的正反馈环，调节膀胱癌的迁移、侵袭和吉西他滨耐药性。
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