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ARTICLE

Loss of TNFRSF21 induces cisplatin sensitivity in lung adenocarcinoma

DAIEN ZHOU1,#, HAOYANG YUAN2,#, YIWEI HU3, CHUXU WANG1, SA GE1, KOUFENG SHAO4, HONGYING WANG1, XIAOFENG TIAN1,*, HAIBO HU1,*
1 Department of Thoracic Surgery, The Affiliated Huai’an Hospital of Xuzhou Medical University, The Second People’s Hospital of Huai’an, Huai’an, 223001, China
2 Medical Faculty, Kunming University of Science and Technology, Kunming, 650000, China
3 The First School of Clinical Medicine, Nanjing Medical University, Nanjing, 210000, China
4 Department of Oncology, Huai’an Chuzhou Hospital of Traditional Chinese Medicine, Zhongda Hospital Group Hospital Affiliated to Southeast University, Huai’an, 223001, China
* Corresponding Author: XIAOFENG TIAN. Email: email; HAIBO HU. Email: email
# These authors contributed equally
(This article belongs to the Special Issue: New Insights in Drug Resistance of Cancer Therapy: A New Wine in an Old Bottle)

Oncology Research https://doi.org/10.32604/or.2024.050182

Received 30 January 2024; Accepted 07 June 2024; Published online 09 September 2024

Abstract

Background: Despite the identification of numerous therapeutic targets in lung cancer, achieving significant efficacy has been challenging. TNFRSF21 plays an important role in various cancers. We investigated the function of TNFRSF21 in lung adenocarcinoma (LUAD). Methods: The prognostic value of TNFRSF21 expression in lung cancer was evaluated by the GEPIA and Kaplan-Meier Plotter databases. Lung cancer cell viability was assessed by the CCK8 assay. TNFRSF21 expression patterns in lung cancer tissues and cells were examined using RT-PCR assay. Tumor sphere growth was evaluated through tumor sphere formation assays. MtROS contents in lung cancer cells were observed through MitoSOX fluorescent assays. Result: TNFRSF21 was up-regulated in LUAD patients. TNFRSF21 induction was particularly notable in LUAD, especially in cancerous cells (A549, H1299, H460, and SPC-A1), compared to BEAS-2B cells. Additionally, TNFRSF21 was increased in cisplatin (DDP)-resistant LUAD cells. Loss of TNFRSF21 significantly inhibited LUAD cell growth. It was observed that forced expression of TNFRSF21 contributed to tumor cell proliferation and DDP resistance. The production of ROS was found to participate in the inhibitory effects on lung cancer stem cells (CSCs), with decreased TNFRSF21 restraining ROS contents. Collectively, these findings reveal that the downregulation of TNFRSF21 promotes ROS contents to restrain the lung CSC-like characteristics via modulation of CD44 and CD133. Conclusions: In conclusion, TNFRSF21 may act as a novel target for lung cancer chemotherapy, particularly for eradicating lung CSCs.

Keywords

TNFRSF21; Lung cancer; Cancer stem cells (CSCs); Cisplatin sensitivity

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