Circular RNA circCPA4 promotes tumorigenesis by regulating miR‐214‐3p/TGIF2 in lung cancer
| Autor: | Decun Zhou, Cheng Cao, Wenhu Tao, Gaofei Ren |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Male
Pulmonary and Respiratory Medicine Lung Neoplasms Carcinogenesis Down-Regulation miR‐214‐3p Apoptosis Treatment of lung cancer medicine.disease_cause Mice Cell Movement Circular RNA Cell Line Tumor TGIF2 Animals Humans Medicine miR-214 Lung cancer RC254-282 Aged Cell Proliferation Homeodomain Proteins Mice Inbred BALB C Gene knockdown business.industry RNA Neoplasms. Tumors. Oncology. Including cancer and carcinogens CircCPA4 Original Articles RNA Circular General Medicine Middle Aged medicine.disease Xenograft Model Antitumor Assays Gene Expression Regulation Neoplastic Repressor Proteins MicroRNAs lung cancer Real-time polymerase chain reaction Oncology Cancer research Original Article Female progression business |
| Zdroj: | Thoracic Cancer, Vol 12, Iss 24, Pp 3356-3369 (2021) Thoracic Cancer |
| ISSN: | 1759-7706 1759-7714 |
| Popis: | Background Lung cancer is the most prevalent malignancy in adults. Circular RNA (circRNA) circCPA4 (hsa_circ_0082374) is highly expressed in non‐small cell lung cancer (NSCLC). The purpose of this study was to explore the role and mechanism of circCPA4 in lung cancer. Methods CircCPA4, linear CPA4, TGF‐β‐induced factor homeobox 2 (TGIF2), and microRNA‐214‐3p (miR‐214‐3p) levels were measured by real‐time quantitative polymerase chain reaction (RT‐qPCR). The protein levels of TGIF2, Beclin1, and p62 were assessed by western blot assay. Colony numbers, migration, invasion, apoptosis, and cell cycle progression were examined by colony formation, wound‐healing, transwell, and flow cytometry assays, respectively. The binding relationship between miR‐214‐3p and circCPA4 or TGIF2 was predicted by StarBase or TargetScan and then verified by a dual‐luciferase reporter, RNA immunoprecipitation (RIP), and RNA pulldown assays. The biological role of circCPA4 on lung tumor growth was assessed by a xenograft tumor model in vivo, and TGIF2 and ki‐67 expression was assessed by immunohistochemistry. Results We determined that CircCPA4 and TGIF2 were increased, and miR‐214‐3p was decreased in lung cancer tissues and cells. Functionally, circCPA4 knockdown could suppress colony formation, migration, invasion, cell cycle progression, and expedite apoptosis of lung cancer cells in vitro. Mechanically, circCPA4 could regulate TGIF2 expression by sponging miR‐214‐3p. In addition, circCPA4 deficiency inhibited the tumor growth in lung cancer in the mouse model. Conclusions CircCPA4 could act as a sponge of miR‐214‐3p to upregulate TGIF2 expression, thereby promoting the progression of lung cancer cells. These findings suggested underlying therapeutic targets for the treatment of lung cancer. Lung cancer is the most prevalent malignancy in adults, and circular RNA (circRNA) circCPA4 (hsa_circ_0082374) is highly expressed in non‐small cell lung cancer. In this paper, our results suggested that circCPA4 deficiency could inhibit the progression of lung cancer cells by regulating the miR‐214‐3p/ TGIF2 axis. These findings suggested underlying therapeutic targets for the treatment of lung cancer. |
| Databáze: | OpenAIRE |
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