HOXC13 promotes cervical cancer proliferation, invasion and Warburg effect through β-catenin/c-Myc signaling pathway
Cervical cancer (CC) is one of the most common malignancy and is the second leading cause of death in gynecologic malignancies worldwide. The homeobox transcription factor homeobox C13 (HOXC13) has been demonstrated to play crucial roles in various cancers. However, its function in CC remains to be...
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description | Cervical cancer (CC) is one of the most common malignancy and is the second leading cause of death in gynecologic malignancies worldwide. The homeobox transcription factor homeobox C13 (HOXC13) has been demonstrated to play crucial roles in various cancers. However, its function in CC remains to be addressed. In the present study, upregulation of HOXC13 expression in human CC tissues was found in The Cancer Genome Atlas (TCGA) dataset and clinical samples and was associated with tumor size, FIGO stage and lymph node metastasis. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot assays suggested that the expression of HOXC13 was up-regulated in CC cells. Cell Counting Kit (CCK)-8, colony formation and cell cycle analysis assays indicated that HOXC13 promoted the proliferation and cycle progression of CC cells in vitro. Of note, knockdown of HOXC13 hinders tumor growth of xenograft tumor mice in vivo. Moreover, transwell and glycolysis measurement assays demonstrated that HOXC13 enhanced the migration, invasion and glycolysis of CC cells in vitro. Further mechanism analysis suggested that HOXC13 participated in CC progression through regulation of the β-catenin/c-Myc signaling pathway. Collectively, HOXC13 facilitated cell proliferation, migration, invasion and glycolysis through modulating β-catenin/c-Myc signaling pathway in CC, indicating that HOXC13 may provide a promising therapeutic target for the therapy of CC.
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doi_str_mv | 10.1007/s10863-021-09908-1 |
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Graphical abstract</description><identifier>ISSN: 0145-479X</identifier><identifier>EISSN: 1573-6881</identifier><identifier>DOI: 10.1007/s10863-021-09908-1</identifier><identifier>PMID: 34309767</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animal Anatomy ; Animal Biochemistry ; Animals ; Assaying ; beta Catenin - metabolism ; Biochemistry ; Bioorganic Chemistry ; c-Myc protein ; Cancer ; Cell cycle ; Cell Line, Tumor ; Cell migration ; Cell proliferation ; Cervical cancer ; Chemistry ; Chemistry and Materials Science ; Cholecystokinin ; Disease Progression ; Female ; Genomes ; Glycolysis ; HeLa Cells ; Heterografts ; Histology ; Homeobox ; Homeodomain Proteins - metabolism ; Humans ; Kinases ; Lymph nodes ; Malignancy ; Metastases ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Morphology ; Myc protein ; Neoplasm Invasiveness ; Organic Chemistry ; Polymerase chain reaction ; Proto-Oncogene Proteins c-myc - metabolism ; Signal transduction ; Signaling ; Tumors ; Up-Regulation ; Uterine Cervical Neoplasms - metabolism ; Uterine Cervical Neoplasms - pathology ; Warburg Effect, Oncologic ; Xenografts ; Xenotransplantation ; β-Catenin</subject><ispartof>Journal of bioenergetics and biomembranes, 2021-10, Vol.53 (5), p.597-608</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021</rights><rights>2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-e3294500a5bc27019d3ef0a783a10b59ab992011f69bf545a0e1d5156d9714fb3</citedby><cites>FETCH-LOGICAL-c375t-e3294500a5bc27019d3ef0a783a10b59ab992011f69bf545a0e1d5156d9714fb3</cites><orcidid>0000-0002-9080-9932</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10863-021-09908-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10863-021-09908-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34309767$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dai, MiMi</creatorcontrib><creatorcontrib>Song, JiaJia</creatorcontrib><creatorcontrib>Wang, LianYun</creatorcontrib><creatorcontrib>Zhou, KeNing</creatorcontrib><creatorcontrib>Shu, Li</creatorcontrib><title>HOXC13 promotes cervical cancer proliferation, invasion and Warburg effect through β-catenin/c-Myc signaling pathway</title><title>Journal of bioenergetics and biomembranes</title><addtitle>J Bioenerg Biomembr</addtitle><addtitle>J Bioenerg Biomembr</addtitle><description>Cervical cancer (CC) is one of the most common malignancy and is the second leading cause of death in gynecologic malignancies worldwide. The homeobox transcription factor homeobox C13 (HOXC13) has been demonstrated to play crucial roles in various cancers. However, its function in CC remains to be addressed. In the present study, upregulation of HOXC13 expression in human CC tissues was found in The Cancer Genome Atlas (TCGA) dataset and clinical samples and was associated with tumor size, FIGO stage and lymph node metastasis. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot assays suggested that the expression of HOXC13 was up-regulated in CC cells. Cell Counting Kit (CCK)-8, colony formation and cell cycle analysis assays indicated that HOXC13 promoted the proliferation and cycle progression of CC cells in vitro. Of note, knockdown of HOXC13 hinders tumor growth of xenograft tumor mice in vivo. Moreover, transwell and glycolysis measurement assays demonstrated that HOXC13 enhanced the migration, invasion and glycolysis of CC cells in vitro. Further mechanism analysis suggested that HOXC13 participated in CC progression through regulation of the β-catenin/c-Myc signaling pathway. Collectively, HOXC13 facilitated cell proliferation, migration, invasion and glycolysis through modulating β-catenin/c-Myc signaling pathway in CC, indicating that HOXC13 may provide a promising therapeutic target for the therapy of CC.
Graphical abstract</description><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Animals</subject><subject>Assaying</subject><subject>beta Catenin - metabolism</subject><subject>Biochemistry</subject><subject>Bioorganic Chemistry</subject><subject>c-Myc protein</subject><subject>Cancer</subject><subject>Cell cycle</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Cervical cancer</subject><subject>Chemistry</subject><subject>Chemistry and Materials Science</subject><subject>Cholecystokinin</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Genomes</subject><subject>Glycolysis</subject><subject>HeLa Cells</subject><subject>Heterografts</subject><subject>Histology</subject><subject>Homeobox</subject><subject>Homeodomain Proteins - metabolism</subject><subject>Humans</subject><subject>Kinases</subject><subject>Lymph nodes</subject><subject>Malignancy</subject><subject>Metastases</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Morphology</subject><subject>Myc protein</subject><subject>Neoplasm Invasiveness</subject><subject>Organic Chemistry</subject><subject>Polymerase chain reaction</subject><subject>Proto-Oncogene Proteins c-myc - metabolism</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Tumors</subject><subject>Up-Regulation</subject><subject>Uterine Cervical Neoplasms - metabolism</subject><subject>Uterine Cervical Neoplasms - pathology</subject><subject>Warburg Effect, Oncologic</subject><subject>Xenografts</subject><subject>Xenotransplantation</subject><subject>β-Catenin</subject><issn>0145-479X</issn><issn>1573-6881</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kcFu1DAQhi0EosvCC3BAlrhwwHQmjuP4iFZAkYp6AdGb5Th21lXWWeyk1b4WD8Iz4WULSBw4eaT55rc9HyHPEd4ggDzPCG3DGVTIQCloGT4gKxSSs6Zt8SFZAdaC1VJdn5EnOd8AQAsCHpMzXnNQspErslxcXW-Q032adtPsMrUu3QZrRmpNLPWxMQbvkpnDFF_TEG9NLhU1sadfTeqWNFDnvbMznbdpWoYt_fGdWTO7GOK5ZZ8OluYwRDOGONC9mbd35vCUPPJmzO7Z_bkmX96_-7y5YJdXHz5u3l4yy6WYmeOVqgWAEZ2tJKDqufNgZMsNQieU6ZSqANE3qvOiFgYc9gJF0yuJte_4mrw65ZZffFtcnvUuZOvG0UQ3LVlXQghey7KNgr78B72ZllSefaRkBVIeN7sm1Ymyaco5Oa_3KexMOmgEfZSiT1J0kaJ_SdFYhl7cRy_dzvV_Rn5bKAA_Abm04uDS37v_E_sT_HeX7Q</recordid><startdate>20211001</startdate><enddate>20211001</enddate><creator>Dai, MiMi</creator><creator>Song, JiaJia</creator><creator>Wang, LianYun</creator><creator>Zhou, KeNing</creator><creator>Shu, Li</creator><general>Springer US</general><general>Springer Nature B.V</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>7QO</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PDBOC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-9080-9932</orcidid></search><sort><creationdate>20211001</creationdate><title>HOXC13 promotes cervical cancer proliferation, invasion and Warburg effect through β-catenin/c-Myc signaling pathway</title><author>Dai, MiMi ; Song, JiaJia ; Wang, LianYun ; Zhou, KeNing ; Shu, Li</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-e3294500a5bc27019d3ef0a783a10b59ab992011f69bf545a0e1d5156d9714fb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Animals</topic><topic>Assaying</topic><topic>beta Catenin - 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Academic</collection><jtitle>Journal of bioenergetics and biomembranes</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dai, MiMi</au><au>Song, JiaJia</au><au>Wang, LianYun</au><au>Zhou, KeNing</au><au>Shu, Li</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HOXC13 promotes cervical cancer proliferation, invasion and Warburg effect through β-catenin/c-Myc signaling pathway</atitle><jtitle>Journal of bioenergetics and biomembranes</jtitle><stitle>J Bioenerg Biomembr</stitle><addtitle>J Bioenerg Biomembr</addtitle><date>2021-10-01</date><risdate>2021</risdate><volume>53</volume><issue>5</issue><spage>597</spage><epage>608</epage><pages>597-608</pages><issn>0145-479X</issn><eissn>1573-6881</eissn><abstract>Cervical cancer (CC) is one of the most common malignancy and is the second leading cause of death in gynecologic malignancies worldwide. The homeobox transcription factor homeobox C13 (HOXC13) has been demonstrated to play crucial roles in various cancers. However, its function in CC remains to be addressed. In the present study, upregulation of HOXC13 expression in human CC tissues was found in The Cancer Genome Atlas (TCGA) dataset and clinical samples and was associated with tumor size, FIGO stage and lymph node metastasis. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot assays suggested that the expression of HOXC13 was up-regulated in CC cells. Cell Counting Kit (CCK)-8, colony formation and cell cycle analysis assays indicated that HOXC13 promoted the proliferation and cycle progression of CC cells in vitro. Of note, knockdown of HOXC13 hinders tumor growth of xenograft tumor mice in vivo. Moreover, transwell and glycolysis measurement assays demonstrated that HOXC13 enhanced the migration, invasion and glycolysis of CC cells in vitro. Further mechanism analysis suggested that HOXC13 participated in CC progression through regulation of the β-catenin/c-Myc signaling pathway. Collectively, HOXC13 facilitated cell proliferation, migration, invasion and glycolysis through modulating β-catenin/c-Myc signaling pathway in CC, indicating that HOXC13 may provide a promising therapeutic target for the therapy of CC.
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subjects | Animal Anatomy Animal Biochemistry Animals Assaying beta Catenin - metabolism Biochemistry Bioorganic Chemistry c-Myc protein Cancer Cell cycle Cell Line, Tumor Cell migration Cell proliferation Cervical cancer Chemistry Chemistry and Materials Science Cholecystokinin Disease Progression Female Genomes Glycolysis HeLa Cells Heterografts Histology Homeobox Homeodomain Proteins - metabolism Humans Kinases Lymph nodes Malignancy Metastases Mice Mice, Inbred BALB C Mice, Nude Morphology Myc protein Neoplasm Invasiveness Organic Chemistry Polymerase chain reaction Proto-Oncogene Proteins c-myc - metabolism Signal transduction Signaling Tumors Up-Regulation Uterine Cervical Neoplasms - metabolism Uterine Cervical Neoplasms - pathology Warburg Effect, Oncologic Xenografts Xenotransplantation β-Catenin |
title | HOXC13 promotes cervical cancer proliferation, invasion and Warburg effect through β-catenin/c-Myc signaling pathway |
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