Propranolol suppresses the proliferation and induces the apoptosis of liver cancer cells
An increasing amount of evidence indicates that the inhibition of β adrenergic signaling can result in the inhibition of tumor growth. However, the role of propranolol in liver cancer and the underlying mechanism remain to be elucidated. The present study aimed to investigate the role of propranolol...
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| Veröffentlicht in: | Molecular medicine reports 2018-04, Vol.17 (4), p.5213-5221 |
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| creator | Wang, Fang Liu, Hui Wang, Fengmei Xu, Ruicheng Wang, Peng Tang, Fei Zhang, Xu Zhu, Zhengyan Lv, Hongmin Han, Tao |
| description | An increasing amount of evidence indicates that the inhibition of β adrenergic signaling can result in the inhibition of tumor growth. However, the role of propranolol in liver cancer and the underlying mechanism remain to be elucidated. The present study aimed to investigate the role of propranolol in liver cancer cell lines and provide evidence for further clinical study. Propranolol was added at different concentrations to HepG2 and HepG2.2.15 liver cancer cells and HL‑7702 normal human liver cells. The proliferation of the cell lines was monitored by live‑cell imaging at a range of time intervals. Immunofluorescence using DAPI and Hoechst 33342/propidium iodide (PI) staining, Annexin V‑FITC/PI double‑staining flow cytometry, western blotting and reverse transcription‑quantitative polymerase chain reaction were used to investigate the effect of propranolol on liver cancer cell apoptosis. The proliferation of HepG2 and HepG2.2.15 cells was inhibited by 40 and 80 µmol/l propranolol. However, the proliferation of HL‑7702 cells was not affected by |
| doi_str_mv | 10.3892/mmr.2018.8476 |
| format | Article |
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However, the role of propranolol in liver cancer and the underlying mechanism remain to be elucidated. The present study aimed to investigate the role of propranolol in liver cancer cell lines and provide evidence for further clinical study. Propranolol was added at different concentrations to HepG2 and HepG2.2.15 liver cancer cells and HL‑7702 normal human liver cells. The proliferation of the cell lines was monitored by live‑cell imaging at a range of time intervals. Immunofluorescence using DAPI and Hoechst 33342/propidium iodide (PI) staining, Annexin V‑FITC/PI double‑staining flow cytometry, western blotting and reverse transcription‑quantitative polymerase chain reaction were used to investigate the effect of propranolol on liver cancer cell apoptosis. The proliferation of HepG2 and HepG2.2.15 cells was inhibited by 40 and 80 µmol/l propranolol. However, the proliferation of HL‑7702 cells was not affected by <160 µmol/l propranolol. Propranolol treatment decreased the expression of adrenergic receptor β‑2 to a greater extent than adrenergic receptor β‑1, and induced apoptosis in the liver cancer cells. The apoptotic rates of HepG2 and HepG2.2.15 cells increased following treatment with propranolol, while the apoptotic rate of HL‑7702 cells was not affected. Propranolol promoted poly (ADP‑ribose) polymerase cleavage and decreased the expression of full‑length caspase‑3 in liver cancer cell lines; it induced S‑phase arrest in HepG2 and HepG2.2.15 cell lines, while HL‑7702 cells were arrested at the G0/G1 phase of the cell cycle. Thus, it was demonstrated that propranolol inhibited proliferation, promoted apoptosis and induced S-phase arrest in HepG2 and HepG2.2.15 cells.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2018.8476</identifier><identifier>PMID: 29393410</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Adrenergic beta-Antagonists - pharmacology ; Adrenergic receptors ; Analysis ; Annexin V ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - genetics ; Biomarkers ; Breast cancer ; Cancer therapies ; Carcinoma, Hepatocellular ; Care and treatment ; Caspase ; Caspase-3 ; Cell cycle ; Cell Cycle - drug effects ; Cell growth ; Cell Line, Tumor ; Cell proliferation ; Cell Proliferation - drug effects ; Diagnosis ; Drug dosages ; Flow Cytometry ; G1 phase ; Hepatocellular carcinoma ; Hepatocytes ; Humans ; Immunofluorescence ; Liver cancer ; Liver cirrhosis ; Liver Neoplasms ; Medical prognosis ; Metastasis ; Mortality ; Physiology ; Polymerase chain reaction ; Propidium iodide ; Propranolol ; Propranolol - pharmacology ; Receptors, Adrenergic, beta-1 - genetics ; Receptors, Adrenergic, beta-1 - metabolism ; Receptors, Adrenergic, beta-2 - genetics ; Receptors, Adrenergic, beta-2 - metabolism ; Reverse transcription ; Ribose ; Studies ; Tumor cell lines ; Western blotting</subject><ispartof>Molecular medicine reports, 2018-04, Vol.17 (4), p.5213-5221</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><rights>Copyright: © Wang et al. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c548t-4879bdff849c4660630263e8934955e5e5f850cdf944fde4e92fe569e596d9733</citedby><cites>FETCH-LOGICAL-c548t-4879bdff849c4660630263e8934955e5e5f850cdf944fde4e92fe569e596d9733</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29393410$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Fang</creatorcontrib><creatorcontrib>Liu, Hui</creatorcontrib><creatorcontrib>Wang, Fengmei</creatorcontrib><creatorcontrib>Xu, Ruicheng</creatorcontrib><creatorcontrib>Wang, Peng</creatorcontrib><creatorcontrib>Tang, Fei</creatorcontrib><creatorcontrib>Zhang, Xu</creatorcontrib><creatorcontrib>Zhu, Zhengyan</creatorcontrib><creatorcontrib>Lv, Hongmin</creatorcontrib><creatorcontrib>Han, Tao</creatorcontrib><title>Propranolol suppresses the proliferation and induces the apoptosis of liver cancer cells</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>An increasing amount of evidence indicates that the inhibition of β adrenergic signaling can result in the inhibition of tumor growth. However, the role of propranolol in liver cancer and the underlying mechanism remain to be elucidated. The present study aimed to investigate the role of propranolol in liver cancer cell lines and provide evidence for further clinical study. Propranolol was added at different concentrations to HepG2 and HepG2.2.15 liver cancer cells and HL‑7702 normal human liver cells. The proliferation of the cell lines was monitored by live‑cell imaging at a range of time intervals. Immunofluorescence using DAPI and Hoechst 33342/propidium iodide (PI) staining, Annexin V‑FITC/PI double‑staining flow cytometry, western blotting and reverse transcription‑quantitative polymerase chain reaction were used to investigate the effect of propranolol on liver cancer cell apoptosis. The proliferation of HepG2 and HepG2.2.15 cells was inhibited by 40 and 80 µmol/l propranolol. However, the proliferation of HL‑7702 cells was not affected by <160 µmol/l propranolol. Propranolol treatment decreased the expression of adrenergic receptor β‑2 to a greater extent than adrenergic receptor β‑1, and induced apoptosis in the liver cancer cells. The apoptotic rates of HepG2 and HepG2.2.15 cells increased following treatment with propranolol, while the apoptotic rate of HL‑7702 cells was not affected. Propranolol promoted poly (ADP‑ribose) polymerase cleavage and decreased the expression of full‑length caspase‑3 in liver cancer cell lines; it induced S‑phase arrest in HepG2 and HepG2.2.15 cell lines, while HL‑7702 cells were arrested at the G0/G1 phase of the cell cycle. Thus, it was demonstrated that propranolol inhibited proliferation, promoted apoptosis and induced S-phase arrest in HepG2 and HepG2.2.15 cells.</description><subject>Adrenergic beta-Antagonists - pharmacology</subject><subject>Adrenergic receptors</subject><subject>Analysis</subject><subject>Annexin V</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>Biomarkers</subject><subject>Breast cancer</subject><subject>Cancer therapies</subject><subject>Carcinoma, Hepatocellular</subject><subject>Care and treatment</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Cell cycle</subject><subject>Cell Cycle - drug effects</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Diagnosis</subject><subject>Drug dosages</subject><subject>Flow Cytometry</subject><subject>G1 phase</subject><subject>Hepatocellular carcinoma</subject><subject>Hepatocytes</subject><subject>Humans</subject><subject>Immunofluorescence</subject><subject>Liver cancer</subject><subject>Liver cirrhosis</subject><subject>Liver Neoplasms</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>Mortality</subject><subject>Physiology</subject><subject>Polymerase chain reaction</subject><subject>Propidium iodide</subject><subject>Propranolol</subject><subject>Propranolol - pharmacology</subject><subject>Receptors, Adrenergic, beta-1 - genetics</subject><subject>Receptors, Adrenergic, beta-1 - metabolism</subject><subject>Receptors, Adrenergic, beta-2 - genetics</subject><subject>Receptors, Adrenergic, beta-2 - metabolism</subject><subject>Reverse transcription</subject><subject>Ribose</subject><subject>Studies</subject><subject>Tumor cell lines</subject><subject>Western blotting</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</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>eNptUk1rFjEQDmKxtXr0KgtevOzbZPOxmYtQil9QqAcFbyHNTtqU3WRNdgv-e7P2tVopc5iQeeaZeWaGkFeM7riG7mSa8q6jTO-06NUTcsR6YC2nVDzdvzuA_pA8L-WGUiU7Cc_IYQccuGD0iHz_ktOcbUxjGpuyznPGUrA0yzU2c05j8JjtElJsbByaEIfV7aN2TvOSSihN8s0YbjE3zka3ORzH8oIceDsWfLn3x-Tbh_dfzz615xcfP5-dnrdOCr20QvdwOXivBTihFFWcdoqjru2BlFjNa0nd4EEIP6BA6DxKBShBDdBzfkze3fHO6-WEg8O4ZDuaOYfJ5p8m2WAeRmK4Nlfp1kitJOi-ErzdE-T0Y8WymCmUTYKNmNZiGNRhAaN8q_XmP-hNWnOs8sy2gsqmmfqLurIjmhB9qnXdRmpOJZcdlxpERe0eQVUbcAouRfSh_j9IaO8SXE6lZPT3Ghk12ymYegq_-zDbKVT8638Hc4_-s3v-C7oYr1Q</recordid><startdate>20180401</startdate><enddate>20180401</enddate><creator>Wang, Fang</creator><creator>Liu, Hui</creator><creator>Wang, Fengmei</creator><creator>Xu, Ruicheng</creator><creator>Wang, Peng</creator><creator>Tang, Fei</creator><creator>Zhang, Xu</creator><creator>Zhu, Zhengyan</creator><creator>Lv, Hongmin</creator><creator>Han, Tao</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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pharmacology</topic><topic>Adrenergic receptors</topic><topic>Analysis</topic><topic>Annexin V</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>Biomarkers</topic><topic>Breast cancer</topic><topic>Cancer therapies</topic><topic>Carcinoma, Hepatocellular</topic><topic>Care and treatment</topic><topic>Caspase</topic><topic>Caspase-3</topic><topic>Cell cycle</topic><topic>Cell Cycle - drug effects</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>Diagnosis</topic><topic>Drug dosages</topic><topic>Flow Cytometry</topic><topic>G1 phase</topic><topic>Hepatocellular carcinoma</topic><topic>Hepatocytes</topic><topic>Humans</topic><topic>Immunofluorescence</topic><topic>Liver cancer</topic><topic>Liver cirrhosis</topic><topic>Liver Neoplasms</topic><topic>Medical prognosis</topic><topic>Metastasis</topic><topic>Mortality</topic><topic>Physiology</topic><topic>Polymerase chain reaction</topic><topic>Propidium iodide</topic><topic>Propranolol</topic><topic>Propranolol - pharmacology</topic><topic>Receptors, Adrenergic, beta-1 - genetics</topic><topic>Receptors, Adrenergic, beta-1 - metabolism</topic><topic>Receptors, Adrenergic, beta-2 - genetics</topic><topic>Receptors, Adrenergic, beta-2 - metabolism</topic><topic>Reverse transcription</topic><topic>Ribose</topic><topic>Studies</topic><topic>Tumor cell lines</topic><topic>Western blotting</topic><toplevel>online_resources</toplevel><creatorcontrib>Wang, Fang</creatorcontrib><creatorcontrib>Liu, Hui</creatorcontrib><creatorcontrib>Wang, Fengmei</creatorcontrib><creatorcontrib>Xu, Ruicheng</creatorcontrib><creatorcontrib>Wang, Peng</creatorcontrib><creatorcontrib>Tang, Fei</creatorcontrib><creatorcontrib>Zhang, Xu</creatorcontrib><creatorcontrib>Zhu, Zhengyan</creatorcontrib><creatorcontrib>Lv, Hongmin</creatorcontrib><creatorcontrib>Han, Tao</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>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 UK/Ireland</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</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>PML(ProQuest Medical Library)</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>Wang, Fang</au><au>Liu, Hui</au><au>Wang, Fengmei</au><au>Xu, Ruicheng</au><au>Wang, Peng</au><au>Tang, Fei</au><au>Zhang, Xu</au><au>Zhu, Zhengyan</au><au>Lv, Hongmin</au><au>Han, Tao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Propranolol suppresses the proliferation and induces the apoptosis of liver cancer cells</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2018-04-01</date><risdate>2018</risdate><volume>17</volume><issue>4</issue><spage>5213</spage><epage>5221</epage><pages>5213-5221</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>An increasing amount of evidence indicates that the inhibition of β adrenergic signaling can result in the inhibition of tumor growth. However, the role of propranolol in liver cancer and the underlying mechanism remain to be elucidated. The present study aimed to investigate the role of propranolol in liver cancer cell lines and provide evidence for further clinical study. Propranolol was added at different concentrations to HepG2 and HepG2.2.15 liver cancer cells and HL‑7702 normal human liver cells. The proliferation of the cell lines was monitored by live‑cell imaging at a range of time intervals. Immunofluorescence using DAPI and Hoechst 33342/propidium iodide (PI) staining, Annexin V‑FITC/PI double‑staining flow cytometry, western blotting and reverse transcription‑quantitative polymerase chain reaction were used to investigate the effect of propranolol on liver cancer cell apoptosis. The proliferation of HepG2 and HepG2.2.15 cells was inhibited by 40 and 80 µmol/l propranolol. However, the proliferation of HL‑7702 cells was not affected by <160 µmol/l propranolol. Propranolol treatment decreased the expression of adrenergic receptor β‑2 to a greater extent than adrenergic receptor β‑1, and induced apoptosis in the liver cancer cells. The apoptotic rates of HepG2 and HepG2.2.15 cells increased following treatment with propranolol, while the apoptotic rate of HL‑7702 cells was not affected. Propranolol promoted poly (ADP‑ribose) polymerase cleavage and decreased the expression of full‑length caspase‑3 in liver cancer cell lines; it induced S‑phase arrest in HepG2 and HepG2.2.15 cell lines, while HL‑7702 cells were arrested at the G0/G1 phase of the cell cycle. Thus, it was demonstrated that propranolol inhibited proliferation, promoted apoptosis and induced S-phase arrest in HepG2 and HepG2.2.15 cells.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>29393410</pmid><doi>10.3892/mmr.2018.8476</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adrenergic beta-Antagonists - pharmacology Adrenergic receptors Analysis Annexin V Apoptosis Apoptosis - drug effects Apoptosis - genetics Biomarkers Breast cancer Cancer therapies Carcinoma, Hepatocellular Care and treatment Caspase Caspase-3 Cell cycle Cell Cycle - drug effects Cell growth Cell Line, Tumor Cell proliferation Cell Proliferation - drug effects Diagnosis Drug dosages Flow Cytometry G1 phase Hepatocellular carcinoma Hepatocytes Humans Immunofluorescence Liver cancer Liver cirrhosis Liver Neoplasms Medical prognosis Metastasis Mortality Physiology Polymerase chain reaction Propidium iodide Propranolol Propranolol - pharmacology Receptors, Adrenergic, beta-1 - genetics Receptors, Adrenergic, beta-1 - metabolism Receptors, Adrenergic, beta-2 - genetics Receptors, Adrenergic, beta-2 - metabolism Reverse transcription Ribose Studies Tumor cell lines Western blotting |
| title | Propranolol suppresses the proliferation and induces the apoptosis of liver cancer cells |
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