Metformin induces apoptosis and inhibits migration by activating the AMPK/p53 axis and suppressing PI3K/AKT signaling in human cervical cancer cells
Human cervical cancer is the fourth most common malignancy among women worldwide, and it is expected to result in 460,000 deaths per year by 2040. Moreover, patients with cervical cancer often display drug resistance and severe side effects; therefore, the development of effective novel chemotherape...
Gespeichert in:
| Veröffentlicht in: | Molecular medicine reports 2021-01, Vol.23 (1), Article 88 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | |
|---|---|
| container_issue | 1 |
| container_start_page | |
| container_title | Molecular medicine reports |
| container_volume | 23 |
| creator | Chen, Ya-Hui Yang, Shun-Fa Yang, Chueh-Ko Tsai, Horng-Der Chen, Tze-Ho Chou, Ming-Chih Hsiao, Yi-Hsuan |
| description | Human cervical cancer is the fourth most common malignancy among women worldwide, and it is expected to result in 460,000 deaths per year by 2040. Moreover, patients with cervical cancer often display drug resistance and severe side effects; therefore, the development of effective novel chemotherapeutic agents is important. In the present study, the effects of metformin, a first‑line therapeutic drug for type 2 diabetes mellitus, were evaluated in cervical cancer. Compared with the control group, metformin significantly inhibited cell viability and migration, and induced apoptosis and cell cycle arrest in human cervical cancer cell lines (CaSki and HeLa). Following metformin treatment, the protein expression levels of p‑AMP‑activated protein kinase (p‑AMPK), which promotes cell death, and the tumor suppressor protein p‑p53 were remarkably upregulated in CaSki and C33A cells compared with the control group. Furthermore, compared with the control group, metformin significantly suppressed the PI3K/AKT signaling pathway in CaSki, C33A and HeLa cells. Compound C (an AMPK inhibitor) significantly reversed the effects of metformin on CaSki, C33A and HeLa cell viability, and AMPK and p53 phosphorylation. The results of the present study suggested that metformin induced AMPK‑mediated apoptosis, thus metformin may serve as a chemotherapeutic agent for human cervical cancer. |
| doi_str_mv | 10.3892/mmr.2020.11725 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7716426</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A647367579</galeid><sourcerecordid>A647367579</sourcerecordid><originalsourceid>FETCH-LOGICAL-c485t-7eddc86252e9f8906f695bf551335e6c00887488e4a1d1892be5fceb348c22843</originalsourceid><addsrcrecordid>eNptUk1v1DAQtRCIloUrR2SJC5fd9bedC9KqolBtK3ooZ8txnF1XiR3sZEX_Bz-4TlnKhyofPDN-741n9AB4i9GKqoqs-z6tCCJohbEk_Bk4xbLCS4oQe36MSVXJE_Aq51uEBCe8eglOKCVUYMpPwc8rN7Yx9T5AH5rJugzNEIcxZl-i0JTq3td-zLD3u2RGHwOs76Cxoz-ULOzguHdwc3W9XQ-cQvPjSMvTMCSX84y4vqDb9WZ7A7PfBdPNpdJuP_UmQOvSwVvTQWtCiUvedfk1eNGaLrs3x3sBvp1_ujn7srz8-vnibHO5tEzxcSld01glCCeualWFRCsqXrecY0q5ExYhpSRTyjGDG1y2VTveWldTpiwhitEF-PhLd5jq3jXWhTGZTg_J9ybd6Wi8_vcl-L3exYOWEgtGRBH4cBRI8fvk8qh7n-cRTHBxypowwbBSovxoAd7_B72NUyrreEApoQhF9A9qZzqnfWhj6WtnUb0RTFIhuawKavUEqpzG9d7G4Fpf6k8RbIo5J9c-zoiRnn2ki4_07CP94KNCePf3Zh7hv41D7wFYR8Py</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2468682303</pqid></control><display><type>article</type><title>Metformin induces apoptosis and inhibits migration by activating the AMPK/p53 axis and suppressing PI3K/AKT signaling in human cervical cancer cells</title><source>Spandidos Publications Journals</source><source>MEDLINE</source><source>EZB Free E-Journals</source><source>Alma/SFX Local Collection</source><creator>Chen, Ya-Hui ; Yang, Shun-Fa ; Yang, Chueh-Ko ; Tsai, Horng-Der ; Chen, Tze-Ho ; Chou, Ming-Chih ; Hsiao, Yi-Hsuan</creator><creatorcontrib>Chen, Ya-Hui ; Yang, Shun-Fa ; Yang, Chueh-Ko ; Tsai, Horng-Der ; Chen, Tze-Ho ; Chou, Ming-Chih ; Hsiao, Yi-Hsuan</creatorcontrib><description>Human cervical cancer is the fourth most common malignancy among women worldwide, and it is expected to result in 460,000 deaths per year by 2040. Moreover, patients with cervical cancer often display drug resistance and severe side effects; therefore, the development of effective novel chemotherapeutic agents is important. In the present study, the effects of metformin, a first‑line therapeutic drug for type 2 diabetes mellitus, were evaluated in cervical cancer. Compared with the control group, metformin significantly inhibited cell viability and migration, and induced apoptosis and cell cycle arrest in human cervical cancer cell lines (CaSki and HeLa). Following metformin treatment, the protein expression levels of p‑AMP‑activated protein kinase (p‑AMPK), which promotes cell death, and the tumor suppressor protein p‑p53 were remarkably upregulated in CaSki and C33A cells compared with the control group. Furthermore, compared with the control group, metformin significantly suppressed the PI3K/AKT signaling pathway in CaSki, C33A and HeLa cells. Compound C (an AMPK inhibitor) significantly reversed the effects of metformin on CaSki, C33A and HeLa cell viability, and AMPK and p53 phosphorylation. The results of the present study suggested that metformin induced AMPK‑mediated apoptosis, thus metformin may serve as a chemotherapeutic agent for human cervical cancer.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2020.11725</identifier><identifier>PMID: 33236135</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; AMP ; AMP-activated protein kinase ; AMP-Activated Protein Kinases - genetics ; AMP-Activated Protein Kinases - metabolism ; Antidiabetics ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - genetics ; Breast cancer ; Cancer therapies ; Cell adhesion & migration ; Cell cycle ; Cell death ; Cell migration ; Cell Movement - drug effects ; Cell Movement - genetics ; Cell viability ; Cervical cancer ; Cervix ; Chemotherapy ; Development and progression ; Diabetes mellitus (non-insulin dependent) ; Drug resistance ; Drug therapy ; Female ; Growth factors ; Health aspects ; HeLa Cells ; Humans ; Insulin ; Kinases ; Laboratories ; Malignancy ; Membranes ; Metformin ; Metformin - pharmacology ; Ovaries ; p53 Protein ; Pancreatic cancer ; Phosphatidylinositol 3-Kinases - genetics ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphorylation ; Physiological aspects ; Prostate ; Protein kinases ; Proteins ; Proto-Oncogene Proteins c-akt - genetics ; Proto-Oncogene Proteins c-akt - metabolism ; Signal transduction ; Signal Transduction - drug effects ; Signal Transduction - genetics ; Tumor cell lines ; Tumor proteins ; Tumor suppressor genes ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism ; Tumors ; Uterine Cervical Neoplasms - drug therapy ; Uterine Cervical Neoplasms - genetics ; Uterine Cervical Neoplasms - metabolism ; Uterine Cervical Neoplasms - pathology</subject><ispartof>Molecular medicine reports, 2021-01, Vol.23 (1), Article 88</ispartof><rights>COPYRIGHT 2021 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2021</rights><rights>Copyright: © Chen et al. 2020</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c485t-7eddc86252e9f8906f695bf551335e6c00887488e4a1d1892be5fceb348c22843</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33236135$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Ya-Hui</creatorcontrib><creatorcontrib>Yang, Shun-Fa</creatorcontrib><creatorcontrib>Yang, Chueh-Ko</creatorcontrib><creatorcontrib>Tsai, Horng-Der</creatorcontrib><creatorcontrib>Chen, Tze-Ho</creatorcontrib><creatorcontrib>Chou, Ming-Chih</creatorcontrib><creatorcontrib>Hsiao, Yi-Hsuan</creatorcontrib><title>Metformin induces apoptosis and inhibits migration by activating the AMPK/p53 axis and suppressing PI3K/AKT signaling in human cervical cancer cells</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Human cervical cancer is the fourth most common malignancy among women worldwide, and it is expected to result in 460,000 deaths per year by 2040. Moreover, patients with cervical cancer often display drug resistance and severe side effects; therefore, the development of effective novel chemotherapeutic agents is important. In the present study, the effects of metformin, a first‑line therapeutic drug for type 2 diabetes mellitus, were evaluated in cervical cancer. Compared with the control group, metformin significantly inhibited cell viability and migration, and induced apoptosis and cell cycle arrest in human cervical cancer cell lines (CaSki and HeLa). Following metformin treatment, the protein expression levels of p‑AMP‑activated protein kinase (p‑AMPK), which promotes cell death, and the tumor suppressor protein p‑p53 were remarkably upregulated in CaSki and C33A cells compared with the control group. Furthermore, compared with the control group, metformin significantly suppressed the PI3K/AKT signaling pathway in CaSki, C33A and HeLa cells. Compound C (an AMPK inhibitor) significantly reversed the effects of metformin on CaSki, C33A and HeLa cell viability, and AMPK and p53 phosphorylation. The results of the present study suggested that metformin induced AMPK‑mediated apoptosis, thus metformin may serve as a chemotherapeutic agent for human cervical cancer.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>AMP</subject><subject>AMP-activated protein kinase</subject><subject>AMP-Activated Protein Kinases - genetics</subject><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>Antidiabetics</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>Breast cancer</subject><subject>Cancer therapies</subject><subject>Cell adhesion & migration</subject><subject>Cell cycle</subject><subject>Cell death</subject><subject>Cell migration</subject><subject>Cell Movement - drug effects</subject><subject>Cell Movement - genetics</subject><subject>Cell viability</subject><subject>Cervical cancer</subject><subject>Cervix</subject><subject>Chemotherapy</subject><subject>Development and progression</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Drug resistance</subject><subject>Drug therapy</subject><subject>Female</subject><subject>Growth factors</subject><subject>Health aspects</subject><subject>HeLa Cells</subject><subject>Humans</subject><subject>Insulin</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Malignancy</subject><subject>Membranes</subject><subject>Metformin</subject><subject>Metformin - pharmacology</subject><subject>Ovaries</subject><subject>p53 Protein</subject><subject>Pancreatic cancer</subject><subject>Phosphatidylinositol 3-Kinases - genetics</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphorylation</subject><subject>Physiological aspects</subject><subject>Prostate</subject><subject>Protein kinases</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - genetics</subject><subject>Tumor cell lines</subject><subject>Tumor proteins</subject><subject>Tumor suppressor genes</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Tumors</subject><subject>Uterine Cervical Neoplasms - drug therapy</subject><subject>Uterine Cervical Neoplasms - genetics</subject><subject>Uterine Cervical Neoplasms - metabolism</subject><subject>Uterine Cervical Neoplasms - pathology</subject><issn>1791-2997</issn><issn>1791-3004</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>eNptUk1v1DAQtRCIloUrR2SJC5fd9bedC9KqolBtK3ooZ8txnF1XiR3sZEX_Bz-4TlnKhyofPDN-741n9AB4i9GKqoqs-z6tCCJohbEk_Bk4xbLCS4oQe36MSVXJE_Aq51uEBCe8eglOKCVUYMpPwc8rN7Yx9T5AH5rJugzNEIcxZl-i0JTq3td-zLD3u2RGHwOs76Cxoz-ULOzguHdwc3W9XQ-cQvPjSMvTMCSX84y4vqDb9WZ7A7PfBdPNpdJuP_UmQOvSwVvTQWtCiUvedfk1eNGaLrs3x3sBvp1_ujn7srz8-vnibHO5tEzxcSld01glCCeualWFRCsqXrecY0q5ExYhpSRTyjGDG1y2VTveWldTpiwhitEF-PhLd5jq3jXWhTGZTg_J9ybd6Wi8_vcl-L3exYOWEgtGRBH4cBRI8fvk8qh7n-cRTHBxypowwbBSovxoAd7_B72NUyrreEApoQhF9A9qZzqnfWhj6WtnUb0RTFIhuawKavUEqpzG9d7G4Fpf6k8RbIo5J9c-zoiRnn2ki4_07CP94KNCePf3Zh7hv41D7wFYR8Py</recordid><startdate>20210101</startdate><enddate>20210101</enddate><creator>Chen, Ya-Hui</creator><creator>Yang, Shun-Fa</creator><creator>Yang, Chueh-Ko</creator><creator>Tsai, Horng-Der</creator><creator>Chen, Tze-Ho</creator><creator>Chou, Ming-Chih</creator><creator>Hsiao, Yi-Hsuan</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</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>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20210101</creationdate><title>Metformin induces apoptosis and inhibits migration by activating the AMPK/p53 axis and suppressing PI3K/AKT signaling in human cervical cancer cells</title><author>Chen, Ya-Hui ; Yang, Shun-Fa ; Yang, Chueh-Ko ; Tsai, Horng-Der ; Chen, Tze-Ho ; Chou, Ming-Chih ; Hsiao, Yi-Hsuan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c485t-7eddc86252e9f8906f695bf551335e6c00887488e4a1d1892be5fceb348c22843</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>AMP</topic><topic>AMP-activated protein kinase</topic><topic>AMP-Activated Protein Kinases - genetics</topic><topic>AMP-Activated Protein Kinases - metabolism</topic><topic>Antidiabetics</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>Breast cancer</topic><topic>Cancer therapies</topic><topic>Cell adhesion & migration</topic><topic>Cell cycle</topic><topic>Cell death</topic><topic>Cell migration</topic><topic>Cell Movement - drug effects</topic><topic>Cell Movement - genetics</topic><topic>Cell viability</topic><topic>Cervical cancer</topic><topic>Cervix</topic><topic>Chemotherapy</topic><topic>Development and progression</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Drug resistance</topic><topic>Drug therapy</topic><topic>Female</topic><topic>Growth factors</topic><topic>Health aspects</topic><topic>HeLa Cells</topic><topic>Humans</topic><topic>Insulin</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>Malignancy</topic><topic>Membranes</topic><topic>Metformin</topic><topic>Metformin - pharmacology</topic><topic>Ovaries</topic><topic>p53 Protein</topic><topic>Pancreatic cancer</topic><topic>Phosphatidylinositol 3-Kinases - genetics</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Phosphorylation</topic><topic>Physiological aspects</topic><topic>Prostate</topic><topic>Protein kinases</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt - genetics</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - genetics</topic><topic>Tumor cell lines</topic><topic>Tumor proteins</topic><topic>Tumor suppressor genes</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Tumors</topic><topic>Uterine Cervical Neoplasms - drug therapy</topic><topic>Uterine Cervical Neoplasms - genetics</topic><topic>Uterine Cervical Neoplasms - metabolism</topic><topic>Uterine Cervical Neoplasms - pathology</topic><toplevel>online_resources</toplevel><creatorcontrib>Chen, Ya-Hui</creatorcontrib><creatorcontrib>Yang, Shun-Fa</creatorcontrib><creatorcontrib>Yang, Chueh-Ko</creatorcontrib><creatorcontrib>Tsai, Horng-Der</creatorcontrib><creatorcontrib>Chen, Tze-Ho</creatorcontrib><creatorcontrib>Chou, Ming-Chih</creatorcontrib><creatorcontrib>Hsiao, Yi-Hsuan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Ya-Hui</au><au>Yang, Shun-Fa</au><au>Yang, Chueh-Ko</au><au>Tsai, Horng-Der</au><au>Chen, Tze-Ho</au><au>Chou, Ming-Chih</au><au>Hsiao, Yi-Hsuan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Metformin induces apoptosis and inhibits migration by activating the AMPK/p53 axis and suppressing PI3K/AKT signaling in human cervical cancer cells</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2021-01-01</date><risdate>2021</risdate><volume>23</volume><issue>1</issue><artnum>88</artnum><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Human cervical cancer is the fourth most common malignancy among women worldwide, and it is expected to result in 460,000 deaths per year by 2040. Moreover, patients with cervical cancer often display drug resistance and severe side effects; therefore, the development of effective novel chemotherapeutic agents is important. In the present study, the effects of metformin, a first‑line therapeutic drug for type 2 diabetes mellitus, were evaluated in cervical cancer. Compared with the control group, metformin significantly inhibited cell viability and migration, and induced apoptosis and cell cycle arrest in human cervical cancer cell lines (CaSki and HeLa). Following metformin treatment, the protein expression levels of p‑AMP‑activated protein kinase (p‑AMPK), which promotes cell death, and the tumor suppressor protein p‑p53 were remarkably upregulated in CaSki and C33A cells compared with the control group. Furthermore, compared with the control group, metformin significantly suppressed the PI3K/AKT signaling pathway in CaSki, C33A and HeLa cells. Compound C (an AMPK inhibitor) significantly reversed the effects of metformin on CaSki, C33A and HeLa cell viability, and AMPK and p53 phosphorylation. The results of the present study suggested that metformin induced AMPK‑mediated apoptosis, thus metformin may serve as a chemotherapeutic agent for human cervical cancer.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>33236135</pmid><doi>10.3892/mmr.2020.11725</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1791-2997 |
| ispartof | Molecular medicine reports, 2021-01, Vol.23 (1), Article 88 |
| issn | 1791-2997 1791-3004 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7716426 |
| source | Spandidos Publications Journals; MEDLINE; EZB Free E-Journals; Alma/SFX Local Collection |
| subjects | 1-Phosphatidylinositol 3-kinase AKT protein AMP AMP-activated protein kinase AMP-Activated Protein Kinases - genetics AMP-Activated Protein Kinases - metabolism Antidiabetics Apoptosis Apoptosis - drug effects Apoptosis - genetics Breast cancer Cancer therapies Cell adhesion & migration Cell cycle Cell death Cell migration Cell Movement - drug effects Cell Movement - genetics Cell viability Cervical cancer Cervix Chemotherapy Development and progression Diabetes mellitus (non-insulin dependent) Drug resistance Drug therapy Female Growth factors Health aspects HeLa Cells Humans Insulin Kinases Laboratories Malignancy Membranes Metformin Metformin - pharmacology Ovaries p53 Protein Pancreatic cancer Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism Phosphorylation Physiological aspects Prostate Protein kinases Proteins Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism Signal transduction Signal Transduction - drug effects Signal Transduction - genetics Tumor cell lines Tumor proteins Tumor suppressor genes Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Tumors Uterine Cervical Neoplasms - drug therapy Uterine Cervical Neoplasms - genetics Uterine Cervical Neoplasms - metabolism Uterine Cervical Neoplasms - pathology |
| title | Metformin induces apoptosis and inhibits migration by activating the AMPK/p53 axis and suppressing PI3K/AKT signaling in human cervical cancer cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-03T14%3A39%3A51IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Metformin%20induces%20apoptosis%20and%20inhibits%20migration%20by%20activating%20the%20AMPK/p53%20axis%20and%20suppressing%20PI3K/AKT%20signaling%20in%20human%20cervical%20cancer%20cells&rft.jtitle=Molecular%20medicine%20reports&rft.au=Chen,%20Ya-Hui&rft.date=2021-01-01&rft.volume=23&rft.issue=1&rft.artnum=88&rft.issn=1791-2997&rft.eissn=1791-3004&rft_id=info:doi/10.3892/mmr.2020.11725&rft_dat=%3Cgale_pubme%3EA647367579%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2468682303&rft_id=info:pmid/33236135&rft_galeid=A647367579&rfr_iscdi=true |