Tim-3 expression in glioma cells is associated with drug resistance
Ji Zhang1, Zheng Quan Zhu2, Yan Xia Li3, Qiu Feng Zhuang1, Yuanhong Lai4, Shao Fang Li4, Xiao Bing Xu5, Jian Min Liu6
1 Department of Neurosurgery, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China
2 Department of Neurosurgery, Tumor Hospital Affiliated of Xinjiang Medical University, Xinshi District, China
3 Department of Rehabilitation, The Second Affiliated Hospital of Xinjiang Medical University, Urumqi, China
4 Department of Urology, State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China
5 Department of Neurosurgery, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde Foshan), Foshan, China
6 Department of Neurosurgery, The First Affiliated Hospital of Guangzhou University of Traditional Chinese Medicine, Guangzhou, China
Xiao Bing Xu
Department of Neurosurgery, Shunde Hospital, Southern Medical University (The First People' s Hospital of Shunde Foshan), Foshan
Source of Support: None, Conflict of Interest: None
Objective: T-cell immunoglobulin and mucin-domain containing-3 (Tim-3) has been widely recognized as a negative regulator of antitumor immunity. However, the mechanism by which Tim-3 suppresses antitumor treatment in gliomas remains unclear. This study aims to explore whether Tim-3 is expressed and to evaluate its effect in drug-fasted glioma cells.
Subjects and Methods: U87 and U251 glioma cell lines were tested. Cell proliferation activity, cell viability, and the protein and mRNA levels of Tim-3 were detected using CCK-8, flow cytometry, Western blotting, and reverse transcription-quantitative polymerase chain reaction, respectively. Enhancement of the sensitivity of glioma cells to chemotherapeutic agents was tested after inhibiting Tim-3 expression using Tim-3 small interfering RNAs (siRNA).
Results: As temozolomide (TMZ) concentration increased, the ratio of apoptotic cells also increased accordingly. However, the level of Tim-3 expression in living cells from the high-dose group was higher than in the low- and middle-dose groups. After interfering with the expression of Tim-3 using siRNA against Tim-3, the killing effect of TMZ rose through an increase in apoptosis.
Conclusions: The presence of Tim-3 mRNA and protein in glioma cells was detected. Significantly, knocking down Tim-3 expression improved the potential of TMZ treatment.