Downregulation of miR‑10b‑5p facilitates the proliferation of uterine leiomyosarcoma cells: A microRNA sequencing‑based approach

Uterine leiomyosarcoma (ULMS) is one of the most aggressive gynecological malignancies. In addition, the molecular background of ULMS has not been fully elucidated due to its low incidence. Therefore, no effective treatment strategies have been established based on its molecular background. The pres...

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Published inOncology reports Vol. 49; no. 5; p. 1
Main Authors Yoshida, Kosuke, Yokoi, Akira, Kitagawa, Masami, Sugiyama, Mai, Yamamoto, Tomofumi, Nakayama, Jun, Yoshida, Hiroshi, Kato, Tomoyasu, Kajiyama, Hiroaki, Yamamoto, Yusuke
Format Journal Article
LanguageEnglish
Published Greece Spandidos Publications 01.05.2023
Spandidos Publications UK Ltd
D.A. Spandidos
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Summary:Uterine leiomyosarcoma (ULMS) is one of the most aggressive gynecological malignancies. In addition, the molecular background of ULMS has not been fully elucidated due to its low incidence. Therefore, no effective treatment strategies have been established based on its molecular background. The present study aimed to investigate the roles of microRNAs (miRNAs/miRs) in the development of ULMS. Comprehensive miRNA sequencing was performed using six ULMS and three myoma samples, and revealed 53 and 11 significantly upregulated and downregulated miRNAs, respectively. One of the most abundant miRNAs in myoma samples was miR‑10b‑5p. The mean normalized read count of miR‑10b‑5p was 93,650 reads in myoma, but only 27,903 reads in ULMS. Subsequently, to investigate the roles of miR‑10b‑5p, gain‑of‑function analysis was performed using SK‑UT‑1 and SK‑LMS‑1 cell lines. The overexpression of miR‑10b‑5p suppressed cell proliferation and reduced the number of colonies. Moreover, miR‑10b‑5p increased the number of cells in the G phase. In conclusion, tumor‑suppressive miR‑10b‑5p was significantly downregulated in ULMS compared with in myoma; thus, miR‑10b‑5p may serve a specific role in sarcoma progression.
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content type line 23
ISSN:1021-335X
1791-2431
DOI:10.3892/or.2023.8523