1. SLCO4A1‐AS1 regulates laryngeal squamous cell carcinoma cell phenotypes via the Wnt pathway
- Author
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Weichun Li, Feng Zhang, Xu Zhang, Linglong Li, Zhongmei He, and Dehong Mao
- Subjects
medicine.diagnostic_test ,Competing endogenous RNA ,Chemistry ,Cell ,Wnt signaling pathway ,030206 dentistry ,Antisense RNA ,Flow cytometry ,03 medical and health sciences ,0302 clinical medicine ,medicine.anatomical_structure ,Otorhinolaryngology ,Downregulation and upregulation ,Apoptosis ,030220 oncology & carcinogenesis ,medicine ,Cancer research ,Signal transduction ,General Dentistry - Abstract
Aim Long noncoding RNAs were widely reported to regulate laryngeal squamous cell carcinoma (LSCC), a prevalent tumor in the head and neck. We aimed to investigate the role of solute carrier organic anion transporter family member 4A1 antisense RNA 1 (SLCO4A1-AS1) in LSCC. Materials & methods CCK-8 and colony formation assays were conducted to examine the viability and proliferation of LSCC cells. The apoptosis of LSCC cells was evaluated using flow cytometry and TUNEL assays. The distribution of SLCO4A1-AS1 in LSCC cells was detected by subcellular fractionation assay. The interaction between molecules was confirmed using luciferase reporter assay. Results SLCO4A1-AS1 was overexpressed in LSCC tissues and cells. Furthermore, silenced SLCO4A1-AS1 repressed the proliferation and facilitated apoptosis of LSCC cells. Mechanistical investigation revealed that SLCO4A1-AS1 was a competing endogenous RNA (ceRNA) to upregulate SETD7 by binding with miR-7855-p. Additionally, SLCO4A1-AS1 positively regulated the Wnt/β-catenin signaling pathway by upregulating SETD7. Rescue experiments demonstrated that SLCO4A1-AS1 promoted LSCC proliferation and inhibited LSCC apoptosis by upregulation of SETD7 and activation of the Wnt/β-catenin pathway. Conclusion SLCO4A1-AS1 promotes proliferation and inhibits apoptosis of LSCC cells by upregulation of SETD7 in a miR-7855-5p dependent way to activate the Wnt/β-catenin pathway.
- Published
- 2021