ITPKA induces cell senescence, inhibits ovarian cancer tumorigenesis and can be downregulated by miR-203
Overcoming senescence is a feature of ovarian cancer cells; however, the mechanisms underlying senescence regulation in ovarian cancer cells remain largely unknown. In this study, we found that ITPKA was downregulated in ovarian cancer samples, and the lower expression correlated with poor survival....
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| Veröffentlicht in: | Aging (Albany, NY.) NY.), 2021-04, Vol.13 (8), p.11822-11832 |
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| creator | Shaosheng, Wang Shaochuang, Wang Lichun, Fan Na, Xie Xiaohong, Zhao |
| description | Overcoming senescence is a feature of ovarian cancer cells; however, the mechanisms underlying senescence regulation in ovarian cancer cells remain largely unknown. In this study, we found that ITPKA was downregulated in ovarian cancer samples, and the lower expression correlated with poor survival. Overexpression of ITPKA inhibited the anchorage-independent growth of ovarian cancer cells and induced senescence. However, knockdown of ITPKA promoted the anchorage-independent growth of ovarian cancer cells and inhibited senescence. Mechanistically, ITPKA was found to interact with MDM2, which stabilized P53, an essential regulator of senescence. Moreover, ITPKA was negatively regulated by miR-203, a microRNA that has been previously reported to be upregulated in ovarian cancer. Taken together, the results of this study demonstrated the tumor suppressive roles of ITPKA in ovarian cancer and provided a good explanation for the oncogenic roles of miR-203. |
| doi_str_mv | 10.18632/aging.202880 |
| format | Article |
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In this study, we found that ITPKA was downregulated in ovarian cancer samples, and the lower expression correlated with poor survival. Overexpression of ITPKA inhibited the anchorage-independent growth of ovarian cancer cells and induced senescence. However, knockdown of ITPKA promoted the anchorage-independent growth of ovarian cancer cells and inhibited senescence. Mechanistically, ITPKA was found to interact with MDM2, which stabilized P53, an essential regulator of senescence. Moreover, ITPKA was negatively regulated by miR-203, a microRNA that has been previously reported to be upregulated in ovarian cancer. 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In this study, we found that ITPKA was downregulated in ovarian cancer samples, and the lower expression correlated with poor survival. Overexpression of ITPKA inhibited the anchorage-independent growth of ovarian cancer cells and induced senescence. However, knockdown of ITPKA promoted the anchorage-independent growth of ovarian cancer cells and inhibited senescence. Mechanistically, ITPKA was found to interact with MDM2, which stabilized P53, an essential regulator of senescence. Moreover, ITPKA was negatively regulated by miR-203, a microRNA that has been previously reported to be upregulated in ovarian cancer. Taken together, the results of this study demonstrated the tumor suppressive roles of ITPKA in ovarian cancer and provided a good explanation for the oncogenic roles of miR-203.</description><subject>Animals</subject><subject>Carcinogenesis - genetics</subject><subject>Cell Line, Tumor</subject><subject>Cellular Senescence - genetics</subject><subject>Down-Regulation</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>HEK293 Cells</subject><subject>Humans</subject><subject>Mice</subject><subject>MicroRNAs - metabolism</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Ovarian Neoplasms - pathology</subject><subject>Ovary - pathology</subject><subject>Phosphotransferases (Alcohol Group Acceptor) - genetics</subject><subject>Research Paper</subject><subject>Up-Regulation</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1945-4589</issn><issn>1945-4589</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkUlPwzAUhC0EoqVw5Ip85ECKl9hNLkgVYqmoBELlbHlrapQ4xU5A_fekC1U5PevNp_HYA8AlRkOccUpuZeF8MSSIZBk6An2cpyxJWZYfH5x74CzGT4Q4Yyk_BT1Ks1HOKe2DxWT29jKGzptW2wi1LUsYrbdRW6_tTScsnHJNhPW3DE56qGW3D7Bpqzq4Yk26CKU3awEqC03944Mt2lI21kC1gpV7Twii5-BkLstoL3ZzAD4eH2b3z8n09WlyP54musvUJBIbxo2UirORoiijNNXazPEo15zqzKKUK6YQI6NUUoxyTYlhLGeaqDQlyNABuNv6LltVWdM9owmyFMvgKhlWopZO_Fe8W4ii_hZZ54YJ6wyudwah_mptbETl4vpfpLd1GwVhmBPCCCYdmmxRHeoYg53vr8FIbNoRm3bEtp2OvzrMtqf_6qC_KEiMkA</recordid><startdate>20210420</startdate><enddate>20210420</enddate><creator>Shaosheng, Wang</creator><creator>Shaochuang, Wang</creator><creator>Lichun, Fan</creator><creator>Na, Xie</creator><creator>Xiaohong, Zhao</creator><general>Impact Journals</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20210420</creationdate><title>ITPKA induces cell senescence, inhibits ovarian cancer tumorigenesis and can be downregulated by miR-203</title><author>Shaosheng, Wang ; Shaochuang, Wang ; Lichun, Fan ; Na, Xie ; Xiaohong, Zhao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c387t-a1d56daab657b308334ccdf179c63c8e046b5b05274a3109c32d5595c2b4420d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Carcinogenesis - genetics</topic><topic>Cell Line, Tumor</topic><topic>Cellular Senescence - genetics</topic><topic>Down-Regulation</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>HEK293 Cells</topic><topic>Humans</topic><topic>Mice</topic><topic>MicroRNAs - metabolism</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Ovarian Neoplasms - pathology</topic><topic>Ovary - pathology</topic><topic>Phosphotransferases (Alcohol Group Acceptor) - genetics</topic><topic>Research Paper</topic><topic>Up-Regulation</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>online_resources</toplevel><creatorcontrib>Shaosheng, Wang</creatorcontrib><creatorcontrib>Shaochuang, Wang</creatorcontrib><creatorcontrib>Lichun, Fan</creatorcontrib><creatorcontrib>Na, Xie</creatorcontrib><creatorcontrib>Xiaohong, Zhao</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Aging (Albany, NY.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shaosheng, Wang</au><au>Shaochuang, Wang</au><au>Lichun, Fan</au><au>Na, Xie</au><au>Xiaohong, Zhao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ITPKA induces cell senescence, inhibits ovarian cancer tumorigenesis and can be downregulated by miR-203</atitle><jtitle>Aging (Albany, NY.)</jtitle><addtitle>Aging (Albany NY)</addtitle><date>2021-04-20</date><risdate>2021</risdate><volume>13</volume><issue>8</issue><spage>11822</spage><epage>11832</epage><pages>11822-11832</pages><issn>1945-4589</issn><eissn>1945-4589</eissn><abstract>Overcoming senescence is a feature of ovarian cancer cells; however, the mechanisms underlying senescence regulation in ovarian cancer cells remain largely unknown. In this study, we found that ITPKA was downregulated in ovarian cancer samples, and the lower expression correlated with poor survival. Overexpression of ITPKA inhibited the anchorage-independent growth of ovarian cancer cells and induced senescence. However, knockdown of ITPKA promoted the anchorage-independent growth of ovarian cancer cells and inhibited senescence. Mechanistically, ITPKA was found to interact with MDM2, which stabilized P53, an essential regulator of senescence. Moreover, ITPKA was negatively regulated by miR-203, a microRNA that has been previously reported to be upregulated in ovarian cancer. Taken together, the results of this study demonstrated the tumor suppressive roles of ITPKA in ovarian cancer and provided a good explanation for the oncogenic roles of miR-203.</abstract><cop>United States</cop><pub>Impact Journals</pub><pmid>33879633</pmid><doi>10.18632/aging.202880</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Carcinogenesis - genetics Cell Line, Tumor Cellular Senescence - genetics Down-Regulation Female Gene Expression Regulation, Neoplastic HEK293 Cells Humans Mice MicroRNAs - metabolism Ovarian Neoplasms - genetics Ovarian Neoplasms - pathology Ovary - pathology Phosphotransferases (Alcohol Group Acceptor) - genetics Research Paper Up-Regulation Xenograft Model Antitumor Assays |
| title | ITPKA induces cell senescence, inhibits ovarian cancer tumorigenesis and can be downregulated by miR-203 |
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