Circular RNA circHECTD1 prevents Diosbulbin-B-sensitivity via miR-137/PBX3 axis in gastric cancer
| Autor: | Guo-Yang Wu, Liang-Hui Li, Long Li, Yi-Zhuo Lu, Guo-Yan Liu |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Cancer Research
Cell miR-137 medicine.disease_cause 03 medical and health sciences 0302 clinical medicine microRNA Genetics medicine Transcription factor RC254-282 030304 developmental biology GC PBX3 0303 health sciences Gene knockdown QH573-671 Oncogene Chemistry Neoplasms. Tumors. Oncology. Including cancer and carcinogens Transfection Molecular biology circHECTD1 mir-137 medicine.anatomical_structure Oncology 030220 oncology & carcinogenesis DB-sensitivity Primary Research Cytology Carcinogenesis |
| Zdroj: | Cancer Cell International, Vol 21, Iss 1, Pp 1-14 (2021) Cancer Cell International |
| ISSN: | 1475-2867 |
| DOI: | 10.1186/s12935-021-01957-1 |
| Popis: | Backgrounds Gastric cancer (GC) is general disease in human digestive system with malignancy. Emerging findings indicated that hsa_circ_0031452 (circHECTD1) was strictly associated with carcinogenesis. Nevertheless, the role of circHECTD1 in drug-resistance still needed to be explained. Methods Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to examine the expression profiles of circHECTD1, microRNA (miR)-137, and pre-leukemia transcription factor 3 (PBX3). The function of circHECTD1 in tumorigenesis was evaluated via xenograft tumor model. The IC50 of Diosbulbin-B (DB) was detected using Cell Counting Kit-8 (CCK8). Cell-cycle and apoptosis were reckoned by flow cytometry. Besides, western blot was administrated to reckon the levels of PBX3 and cell apoptotic indicators. Moreover, the interrelation between miR-137 and circHECTD1 or PBX3 was expounded by dual-luciferase reporter, RNA immunoprecipitation (RIP) and RNA pull down assays. Results We uncovered that circHECTD1 was ectopically up-regulated in GC tissues and cells. CircHECTD1 deficiency sensitized DB-treatment in DB-evoked AGS and HGC-27 cells. In vivo assay, circHECTD1 silencing led to the tumor reduction. Also, circHECTD1 served as miR-137 sponge in a sequence-complementary manner. Furthermore, transfection of miR-137 inhibitor markedly eliminated circHECTD1 absence-mediated promotion of DB-sensitivity in GC cells. Moreover, PBX3, a target of miR-137, play a DB-resistant role in GC cells. Fascinatingly, the deletion of PBX3 reversed the impact of miR-137 repression and circHECTD1 knockdown on DB-sensitivity in vitro. Conclusions CircHECTD1 served as an oncogene by a novel miR-137/PBX3 axis, which might supply an underlying biomarker for the diagnosis and prognosis of GC management. |
| Databáze: | OpenAIRE |
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