Follicle-Stimulating Hormone Promotes the Development of Endometrial Cancer In Vitro and In Vivo
Endocrine disruptors as risk factors for endometrial cancer (EC) are positively correlated with serum follicle-stimulating hormone (FSH) levels. Additionally, increased FSH is associated with EC. However, its exact mechanism is not yet clear. Therefore, this study investigated how FSH affects the oc...
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description | Endocrine disruptors as risk factors for endometrial cancer (EC) are positively correlated with serum follicle-stimulating hormone (FSH) levels. Additionally, increased FSH is associated with EC. However, its exact mechanism is not yet clear. Therefore, this study investigated how FSH affects the occurrence of EC. Using immunohistochemistry (IHC), immunofluorescence (IF), and Western blot (WB), we found that FSH receptor (FSHR) was expressed in both EC tissues and cell lines. To explore the effect of FSH on EC
, Ishikawa (ISK) cells were cultured in different doses of FSH, and it was found that FSH could promote the proliferation and migration of ISK cells. Furthermore, the detection of key molecules of migration and apoptosis by WB showed that FSH promoted cell migration and inhibited apoptosis. Additionally, FSH decreased AMPK activation. To clarify the effect of FSH on EC
, we subcutaneously planted ISK cells into ovariectomized mice and then gave two of the groups oestradiol (E2). In comparison with the OE (ovariectomy plus E2) and sham groups, the growth rates and weights of the tumors in the OE plus FSH group were significantly higher. The findings above suggest that FSH promotes the proliferation and metastasis of EC, providing a new strategy for the treatment of EC. |
doi_str_mv | 10.3390/ijerph192215344 |
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, Ishikawa (ISK) cells were cultured in different doses of FSH, and it was found that FSH could promote the proliferation and migration of ISK cells. Furthermore, the detection of key molecules of migration and apoptosis by WB showed that FSH promoted cell migration and inhibited apoptosis. Additionally, FSH decreased AMPK activation. To clarify the effect of FSH on EC
, we subcutaneously planted ISK cells into ovariectomized mice and then gave two of the groups oestradiol (E2). In comparison with the OE (ovariectomy plus E2) and sham groups, the growth rates and weights of the tumors in the OE plus FSH group were significantly higher. The findings above suggest that FSH promotes the proliferation and metastasis of EC, providing a new strategy for the treatment of EC.</description><identifier>ISSN: 1660-4601</identifier><identifier>ISSN: 1661-7827</identifier><identifier>EISSN: 1660-4601</identifier><identifier>DOI: 10.3390/ijerph192215344</identifier><identifier>PMID: 36430063</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Animals ; Antibiotics ; Antibodies ; Apoptosis ; Cancer therapies ; Cell culture ; Cell Movement ; Cell proliferation ; Chemotherapy ; Disease ; Endocrine disruptors ; Endocrine therapy ; Endometrial cancer ; Endometrial Neoplasms ; Endometrium ; Estrogens ; Female ; Follicle Stimulating Hormone - metabolism ; Follicle-stimulating hormone ; Follicles ; Histology ; Humans ; Immunofluorescence ; Immunohistochemistry ; Kinases ; Medical research ; Metabolism ; Metastases ; Mice ; Middle age ; Ovariectomy ; Ovaries ; Plant cells ; Pollutants ; Proteins ; Risk analysis ; Risk factors ; Tumors ; Womens health</subject><ispartof>International journal of environmental research and public health, 2022-11, Vol.19 (22), p.15344</ispartof><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-7911065b62ee2c4f7ca5b5971ef40e2614ae25c4f61719137dd84794f9d233</citedby><cites>FETCH-LOGICAL-c421t-7911065b62ee2c4f7ca5b5971ef40e2614ae25c4f61719137dd84794f9d233</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9696221/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9696221/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36430063$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sheng, Shuman</creatorcontrib><creatorcontrib>Liu, Wei</creatorcontrib><creatorcontrib>Xue, Yafei</creatorcontrib><creatorcontrib>Pan, Zhengwu</creatorcontrib><creatorcontrib>Zhao, Lanlan</creatorcontrib><creatorcontrib>Wang, Fei</creatorcontrib><creatorcontrib>Qi, Xiaoyi</creatorcontrib><title>Follicle-Stimulating Hormone Promotes the Development of Endometrial Cancer In Vitro and In Vivo</title><title>International journal of environmental research and public health</title><addtitle>Int J Environ Res Public Health</addtitle><description>Endocrine disruptors as risk factors for endometrial cancer (EC) are positively correlated with serum follicle-stimulating hormone (FSH) levels. Additionally, increased FSH is associated with EC. However, its exact mechanism is not yet clear. Therefore, this study investigated how FSH affects the occurrence of EC. Using immunohistochemistry (IHC), immunofluorescence (IF), and Western blot (WB), we found that FSH receptor (FSHR) was expressed in both EC tissues and cell lines. To explore the effect of FSH on EC
, Ishikawa (ISK) cells were cultured in different doses of FSH, and it was found that FSH could promote the proliferation and migration of ISK cells. Furthermore, the detection of key molecules of migration and apoptosis by WB showed that FSH promoted cell migration and inhibited apoptosis. Additionally, FSH decreased AMPK activation. To clarify the effect of FSH on EC
, we subcutaneously planted ISK cells into ovariectomized mice and then gave two of the groups oestradiol (E2). In comparison with the OE (ovariectomy plus E2) and sham groups, the growth rates and weights of the tumors in the OE plus FSH group were significantly higher. The findings above suggest that FSH promotes the proliferation and metastasis of EC, providing a new strategy for the treatment of EC.</description><subject>Animals</subject><subject>Antibiotics</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Cancer therapies</subject><subject>Cell culture</subject><subject>Cell Movement</subject><subject>Cell proliferation</subject><subject>Chemotherapy</subject><subject>Disease</subject><subject>Endocrine disruptors</subject><subject>Endocrine therapy</subject><subject>Endometrial cancer</subject><subject>Endometrial Neoplasms</subject><subject>Endometrium</subject><subject>Estrogens</subject><subject>Female</subject><subject>Follicle Stimulating Hormone - metabolism</subject><subject>Follicle-stimulating hormone</subject><subject>Follicles</subject><subject>Histology</subject><subject>Humans</subject><subject>Immunofluorescence</subject><subject>Immunohistochemistry</subject><subject>Kinases</subject><subject>Medical research</subject><subject>Metabolism</subject><subject>Metastases</subject><subject>Mice</subject><subject>Middle age</subject><subject>Ovariectomy</subject><subject>Ovaries</subject><subject>Plant cells</subject><subject>Pollutants</subject><subject>Proteins</subject><subject>Risk analysis</subject><subject>Risk factors</subject><subject>Tumors</subject><subject>Womens health</subject><issn>1660-4601</issn><issn>1661-7827</issn><issn>1660-4601</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkc1rGzEQxUVJqdO0596CIJdcNtHXaq1LIDjOBwRa2tKrKu_O2jJayZG0hvz3VbETnJxGw_vpaUYPoW-UXHCuyKVdQ9ysqGKM1lyID-iYSkkqIQk9OjhP0OeU1oTwqZDqE5pwKTghkh-jv7fBOds6qH5lO4zOZOuX-D7EIXjAP2IYQoaE8wrwDWzBhc0APuPQ47nvwgA5WuPwzPgWIn7w-I_NMWDju12zDV_Qx964BF_39QT9vJ3_nt1Xj9_vHmbXj1UrGM1Voyglsl5IBsBa0TetqRe1aij0ggCTVBhgdREkbaiivOm6qWiU6FXHOD9BVzvTzbgYoGvLiNE4vYl2MPFZB2P1W8XblV6GrVZSyfJ3xeB8bxDD0wgp68GmFpwzHsKYNGsEqcurkhT07B26DmP0ZbdCcSWYEg0r1OWOamNIKUL_Ogwl-n90-l105cbp4Q6v_EtW_B_SHpXl</recordid><startdate>20221120</startdate><enddate>20221120</enddate><creator>Sheng, Shuman</creator><creator>Liu, Wei</creator><creator>Xue, Yafei</creator><creator>Pan, Zhengwu</creator><creator>Zhao, Lanlan</creator><creator>Wang, Fei</creator><creator>Qi, Xiaoyi</creator><general>MDPI AG</general><general>MDPI</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20221120</creationdate><title>Follicle-Stimulating Hormone Promotes the Development of Endometrial Cancer In Vitro and In Vivo</title><author>Sheng, Shuman ; 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Additionally, increased FSH is associated with EC. However, its exact mechanism is not yet clear. Therefore, this study investigated how FSH affects the occurrence of EC. Using immunohistochemistry (IHC), immunofluorescence (IF), and Western blot (WB), we found that FSH receptor (FSHR) was expressed in both EC tissues and cell lines. To explore the effect of FSH on EC
, Ishikawa (ISK) cells were cultured in different doses of FSH, and it was found that FSH could promote the proliferation and migration of ISK cells. Furthermore, the detection of key molecules of migration and apoptosis by WB showed that FSH promoted cell migration and inhibited apoptosis. Additionally, FSH decreased AMPK activation. To clarify the effect of FSH on EC
, we subcutaneously planted ISK cells into ovariectomized mice and then gave two of the groups oestradiol (E2). In comparison with the OE (ovariectomy plus E2) and sham groups, the growth rates and weights of the tumors in the OE plus FSH group were significantly higher. The findings above suggest that FSH promotes the proliferation and metastasis of EC, providing a new strategy for the treatment of EC.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>36430063</pmid><doi>10.3390/ijerph192215344</doi><oa>free_for_read</oa></addata></record> |
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subjects | Animals Antibiotics Antibodies Apoptosis Cancer therapies Cell culture Cell Movement Cell proliferation Chemotherapy Disease Endocrine disruptors Endocrine therapy Endometrial cancer Endometrial Neoplasms Endometrium Estrogens Female Follicle Stimulating Hormone - metabolism Follicle-stimulating hormone Follicles Histology Humans Immunofluorescence Immunohistochemistry Kinases Medical research Metabolism Metastases Mice Middle age Ovariectomy Ovaries Plant cells Pollutants Proteins Risk analysis Risk factors Tumors Womens health |
title | Follicle-Stimulating Hormone Promotes the Development of Endometrial Cancer In Vitro and In Vivo |
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