IRF4-activated TEX41 promotes the malignant behaviors of melanoma cells by targeting miR-103a-3p/C1QB axis
- BMC Cancer. 2021 Dec 16;21(1):1339. doi: 10.1186/s12885-021-09039-1.
- 1. Department of Dermatology, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, People's Hospital of Henan University, 450003, Zhengzhou, Henan, China.
- 2. Department of Dermatology, Xianyang Central Hospital, No.78, Renmin Road, 712000, Xianyang, Shaanxi, China. [email protected].
- 3. Department of Plastic and Burn Surgery, West China Hospital, West China School of Medicine, Sichuan University, 610041, Chengdu, Sichuan, China.
Background: Malignant Melanoma is an aggressive skin Cancer and a tumor of melanocytic origin. Recent studies have suggested that long non-coding RNAs (lncRNAs) play crucial regulatory roles in multiple malignancies, including Melanoma. Testis expressed 41 (TEX41) is a relatively new lncRNA whose mechanism in Melanoma remains vague.
Aims: This study aimed to explore the role and specific mechanism of TEX41 in Melanoma.
Methods: The expression of genes involved in this study was determined by qRT-PCR. Functional assays were conducted to analyze the role of relevant genes in Melanoma cells. The interaction between TEX41 promoter and IRF4 as well as the relationship among TEX41, miR-103a-3p and C1QB was verified by mechanism assays.
Results: IRF4 up-regulated TEX41 at the transcriptional level in Melanoma cells. TEX41 knockdown hindered Melanoma cell proliferation, migration and invasion while promoting cell Apoptosis. TEX41 bound to miR-103a-3p and regulated C1QB. The suppressive impact of TEX41 depletion on Melanoma cell malignant behaviors could be counteracted by miR-103a-3p inhibition or C1QB overexpression. Moreover, IRF4 could facilitate Melanoma cell growth via up-regulating C1QB.
Conclusions: IRF4-activated TEX41 sequestered miR-103a-3p and modulated C1QB to promote Melanoma cell malignant behaviors, for which TEX41 might be regarded as a potential therapeutic target for Melanoma.
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