Lomerizine Promotes Ferroptosis by Targeting CACNA1b Mediated JAK2/STAT3 Pathway Activation and Reverses Cisplatin Resistance of HNSCC

Author:

Xiao Ting,Zhang Zihui,Tian Jiao,Gu Xiaoting,Li Bing,Xiao Kaidi,Cai Yutian,Li Chengxia,Shan Changliang,Liu Chaoge,Ai Xiaoyu,Zhou Honggang,Yang Cheng

Publisher

Elsevier BV

Reference28 articles.

1. In vivo, we established a nude mouse model of transplanted tumors using CAL-27 cells and CAL-27 cells with knocked down CACNA1B, and treated them with Lomerizine. Compared to the Cal-27 group, treatment with Lomerizine and knockdown of CACNA1B expression significantly inhibited the growth of Cal-27 tumors, while Lomerizine treatment (60mg/kg) in shCACNA1B mice did not significantly reduce tumor volume (figure. 8A-C). Lomerizine and knocking down CACNA1B had no significant effect on the body weight of mice (figure. 8D). The IHC results of mouse tumor tissues showed that knocking down the expression of CACNA1B significantly inhibited the phosphorylation of JAK2;P-Stat3 ; D;GPX

2. Interleukin-6 mediated inflammasome activation promotes oral squamous cell carcinoma progression via JAK2/STAT3/Sox4/NLRP3 signaling pathway;L Xiao;Journal of Experimental & Clinical Cancer Research,2022

3. Energy-Stress-Mediated AMPK Activation Promotes GPX4-Dependent Ferroptosis through the JAK2/STAT3/P53 Axis in Renal Cancer;Y Li;Oxidative Medicine and Cellular Longevity,2022

4. Human colorectal cancer-derived mesenchymal stem cells promote colorectal cancer progression through IL-6/JAK2/STAT3 signaling;X Zhang;Cell Death & Disease,2018

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