PMID- 34659819 OWN - NLM STAT- PubMed-not-MEDLINE LR - 20220816 IS - 2072-1439 (Print) IS - 2077-6624 (Electronic) IS - 2072-1439 (Linking) VI - 13 IP - 9 DP - 2021 Sep TI - miR-488-5p promotes esophageal squamous cell carcinoma progression by suppressing the P53 pathway. PG - 5534-5545 LID - 10.21037/jtd-21-1448 [doi] AB - BACKGROUND: miR-488-3p has been reported to play an important role in cancer progression and metastasis. The protein 53 (P53) gene serves as a mediator and biomarker of esophageal squamous cell carcinoma (ESCC). However, the molecular mechanism underlying miR-488-5p in the pathology of ESCC through the P53 pathway has not been examined. METHODS: The expression levels of miR-488-5p were determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Cytological experiments were performed to evaluate the biological functions of miR-488-5p. A bioinformatics analysis was performed to determine the pathways and key miR-488-5p targets associated with ESCC. Correlations between miR-488-5p and P53 signaling pathways were validated by western blotting and the dual luciferase reporter gene system. Finally, the expression level of miR-488-5p was regulated and tumor formation experiments were performed in nude mice. RESULTS: The qRT-PCR analysis showed that MiR-488-5p expression was more upregulated in the KYSE-150 group than the HEEC group. In the KYSE-150 cells, the colony formation assay and flow cytometry analysis indicated that the miR-488-5p inhibitor inhibited cell viability and increased cell apoptosis; however, these effects were recovered by P53 knockdown (KD). In addition, cell invasion and cell migration were inhibited by the miR-488-5p inhibitor, but were also improved by P53 KD. Similarly, the miR-488-5p inhibitor induced the expression of P53 and P21 than normal control (NC) group in which miR-488-5p expression was normal, while P53 KD prevented the effects of the miR-488-5p inhibitor in KYSE-150 cells. Additionally, we found that tumor size was obviously smaller in miR-488-5p overexpression (OE)+ P53 OE mice than miR-488-5p OE mice. Hematoxylin and eosin and immunohistochemistry staining also revealed similar results. CONCLUSIONS: Our results suggest that miR-488-5p promotes ESCC progression by suppressing the P53 pathway. These findings should provide novel ideas for ESCC therapies. CI - 2021 Journal of Thoracic Disease. All rights reserved. FAU - Su, Chang AU - Su C AD - Department of Thoracic Surgery, Fourth Hospital, Hebei Medical University, Shijiazhuang, China. AD - Department of Cardiothoracic Surgery, Bethune International Peace Hospital, Shijiazhuang, China. FAU - Liu, Wenxiu AU - Liu W AD - Department of Cardiology, Bethune International Peace Hospital, Shijiazhuang, China. FAU - Jiang, Tao AU - Jiang T AD - Department of Thoracic Surgery, Fourth Hospital, Hebei Medical University, Shijiazhuang, China. FAU - Liu, Junfeng AU - Liu J AD - Department of Thoracic Surgery, Fourth Hospital, Hebei Medical University, Shijiazhuang, China. LA - eng PT - Journal Article PL - China TA - J Thorac Dis JT - Journal of thoracic disease JID - 101533916 PMC - PMC8482336 OTO - NOTNLM OT - KYSE-150 OT - P53 OT - esophageal squamous cell carcinoma (ESCC) OT - miR-488-5p COIS- Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://dx.doi.org/10.21037/jtd-21-1448). The authors have no conflicts of interest to declare. EDAT- 2021/10/19 06:00 MHDA- 2021/10/19 06:01 PMCR- 2021/09/01 CRDT- 2021/10/18 09:01 PHST- 2021/07/23 00:00 [received] PHST- 2021/09/17 00:00 [accepted] PHST- 2021/10/18 09:01 [entrez] PHST- 2021/10/19 06:00 [pubmed] PHST- 2021/10/19 06:01 [medline] PHST- 2021/09/01 00:00 [pmc-release] AID - jtd-13-09-5534 [pii] AID - 10.21037/jtd-21-1448 [doi] PST - ppublish SO - J Thorac Dis. 2021 Sep;13(9):5534-5545. doi: 10.21037/jtd-21-1448.