Knockdown of RBM15 inhibits tumor progression and the JAK-STAT signaling pathway in cervical cancer
Abstract Background RNA binding motif protein 15 (RBM15), a writer of N6-methyladenosine (m6A) methylation, contributes significantly to the development of various tumors. However, the function of RBM15 in cervical cancer (CC) has not been determined. Methods Based on the GSE9750, GSE63514, and m6A...
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| Format: | Article |
| Language: | English |
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BMC
2023-07-01
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| Series: | BMC Cancer |
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| Online Access: | https://doi.org/10.1186/s12885-023-11163-z |
| _version_ | 1827895079239417856 |
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| author | Chunnian Zhang Liqin Gu Juan Xiao Feng Jin |
| author_facet | Chunnian Zhang Liqin Gu Juan Xiao Feng Jin |
| author_sort | Chunnian Zhang |
| collection | DOAJ |
| description | Abstract Background RNA binding motif protein 15 (RBM15), a writer of N6-methyladenosine (m6A) methylation, contributes significantly to the development of various tumors. However, the function of RBM15 in cervical cancer (CC) has not been determined. Methods Based on the GSE9750, GSE63514, and m6A datasets, m6A-related differentially expressed genes (DEGs) were screened out. The hub genes were identified by generating a Protein-Protein Interaction (PPI) network. RT-qPCR was conducted to assess the mRNA expression of hub genes. CCK8, scratch wound healing, and transwell assays were utilized to examine the influence of RBM15 on HeLa and SiHa cells. Tumor xenograft models were used to assess the effects of RBM15 on tumorigenesis. A mechanistic analysis of RBM15 in CC tumors was conducted using the GeneCards and Coxpresdb databases, followed by a Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and the pathway-related genes were subsequently validated using Western blotting. Results Five DEGs were screened, including WTAP, RBM15, CBLL1, and YTHDC2. Among them, WTAP, RBM15, CBLL1, and YTHDC2 were hub genes and can be used as biomarkers for CC. RBM15 expression was considerably increased, while WTAP, CBLL1, and YTHDC2 were significantly downregulated. Knockdown of RBM15 significantly suppressed the proliferation, invasion, and migration of CC cells and tumorigenesis. Moreover, knockdown of RBM15 significantly reduced the expression levels of proteins related to the JAK-STAT pathway. Conclusions Knockdown of RBM15 inhibited the progression of CC cells, which probably by inhibiting the JAK-STAT pathway pathway. |
| first_indexed | 2024-03-12T22:16:31Z |
| format | Article |
| id | doaj.art-0efe7cd19c554a7dab3028b1ffdaa7c3 |
| institution | Directory Open Access Journal |
| issn | 1471-2407 |
| language | English |
| last_indexed | 2024-03-12T22:16:31Z |
| publishDate | 2023-07-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Cancer |
| spelling | doaj.art-0efe7cd19c554a7dab3028b1ffdaa7c32023-07-23T11:17:06ZengBMCBMC Cancer1471-24072023-07-0123111310.1186/s12885-023-11163-zKnockdown of RBM15 inhibits tumor progression and the JAK-STAT signaling pathway in cervical cancerChunnian Zhang0Liqin Gu1Juan Xiao2Feng Jin3Department of Gynecology, Ganzhou People’s HospitalDepartment of Gynecology, Ganzhou People’s HospitalDepartment of Gynecology, Ganzhou People’s HospitalDepartment of Gynecology, Ganzhou People’s HospitalAbstract Background RNA binding motif protein 15 (RBM15), a writer of N6-methyladenosine (m6A) methylation, contributes significantly to the development of various tumors. However, the function of RBM15 in cervical cancer (CC) has not been determined. Methods Based on the GSE9750, GSE63514, and m6A datasets, m6A-related differentially expressed genes (DEGs) were screened out. The hub genes were identified by generating a Protein-Protein Interaction (PPI) network. RT-qPCR was conducted to assess the mRNA expression of hub genes. CCK8, scratch wound healing, and transwell assays were utilized to examine the influence of RBM15 on HeLa and SiHa cells. Tumor xenograft models were used to assess the effects of RBM15 on tumorigenesis. A mechanistic analysis of RBM15 in CC tumors was conducted using the GeneCards and Coxpresdb databases, followed by a Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and the pathway-related genes were subsequently validated using Western blotting. Results Five DEGs were screened, including WTAP, RBM15, CBLL1, and YTHDC2. Among them, WTAP, RBM15, CBLL1, and YTHDC2 were hub genes and can be used as biomarkers for CC. RBM15 expression was considerably increased, while WTAP, CBLL1, and YTHDC2 were significantly downregulated. Knockdown of RBM15 significantly suppressed the proliferation, invasion, and migration of CC cells and tumorigenesis. Moreover, knockdown of RBM15 significantly reduced the expression levels of proteins related to the JAK-STAT pathway. Conclusions Knockdown of RBM15 inhibited the progression of CC cells, which probably by inhibiting the JAK-STAT pathway pathway.https://doi.org/10.1186/s12885-023-11163-zCervical cancerN6-methyladenosineRBM15The JAK-STAT signaling pathway |
| spellingShingle | Chunnian Zhang Liqin Gu Juan Xiao Feng Jin Knockdown of RBM15 inhibits tumor progression and the JAK-STAT signaling pathway in cervical cancer BMC Cancer Cervical cancer N6-methyladenosine RBM15 The JAK-STAT signaling pathway |
| title | Knockdown of RBM15 inhibits tumor progression and the JAK-STAT signaling pathway in cervical cancer |
| title_full | Knockdown of RBM15 inhibits tumor progression and the JAK-STAT signaling pathway in cervical cancer |
| title_fullStr | Knockdown of RBM15 inhibits tumor progression and the JAK-STAT signaling pathway in cervical cancer |
| title_full_unstemmed | Knockdown of RBM15 inhibits tumor progression and the JAK-STAT signaling pathway in cervical cancer |
| title_short | Knockdown of RBM15 inhibits tumor progression and the JAK-STAT signaling pathway in cervical cancer |
| title_sort | knockdown of rbm15 inhibits tumor progression and the jak stat signaling pathway in cervical cancer |
| topic | Cervical cancer N6-methyladenosine RBM15 The JAK-STAT signaling pathway |
| url | https://doi.org/10.1186/s12885-023-11163-z |
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