Ganoderma microsporum immunomodulatory protein induces apoptosis and potentiates mitomycin C‐induced apoptosis in urinary bladder urothelial carcinoma cells
Current chemotherapy and immunotherapy treatments followed by transurethral resection for urinary bladder urothelial carcinoma (UC) usually suffer from poor prognosis and high recurrence rate. Design and modification of current formulation with the novel adjuvants are needed. A recombinant protein d...
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| Veröffentlicht in: | Journal of cellular biochemistry 2018-06, Vol.119 (6), p.4592-4606 |
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| creator | Huang, Sheng‐Yuan Chien, Chih‐Cheng Hseu, Ruey‐Shyang Huang, Victoria Ying Jen Chiang, Shang Ying Huang, Chi‐Jung Chen, Shao‐Kuan Tsai, Ru‐Yin Lin, Hsi‐Ting Cheng, Yu‐Che |
| description | Current chemotherapy and immunotherapy treatments followed by transurethral resection for urinary bladder urothelial carcinoma (UC) usually suffer from poor prognosis and high recurrence rate. Design and modification of current formulation with the novel adjuvants are needed. A recombinant protein derived from Ganoderma microsporum named as Ganoderma microsporum immunomodulatory protein (GMIP) was used to treat UC cells. We found GMIP elicits a dose‐dependent and time‐dependent anti‐UC cell proliferation effect, with a half‐maximal inhibition concentration (IC50) comparable to mitomycin C (MMC), a commonly used chemotherapy agent. After GMIP treatment, UC cells showed apoptotic phenomenon including cell cycle arrest in the G1 phase, elevated sub‐G1 population, mitochondrial membrane potential loss, up‐regulated p21 expression, p21 nuclear translocation, caspase activation, and PARP cleavage in a p53‐independent but p21‐mediated pathways. Unlike lung cancer cells, GMIP treated UC cells showed no autophagic scheme including Beclin‐1, an autophagy to apoptosis switch marker, was not cleaved by caspase 3 and slight LC3B‐II accumulation. Also, the classic autophagic inhibitor, chloroquine had no effect in GMIP‐mediated cell death made us conclude that GMIP induced apoptosis through caspase activation but not autophagy in UC cells. Additionally, GMIP showed synergistic effects with MMC in killing UC cells and thus decreased the concentration of MMC usage to reach the comparable apoptotic effects. Our results delineate novel strategies for treatment of UC by GMIP alone or in combination with MMC application and provide a promising therapeutic cocktail for better treatment of urinary bladder urothelial carcinoma.
Ganoderma microsporum immunomodulatory protein (GMIP) showed anti‐ urothelial carcinoma (UC) cell proliferation effect and classical apoptotic phenomenon in a p53‐independent but p21‐mediated manner. GMIP showed synergistic effects with Mitomycin C (MMC) in killing UC cells. Our results delineate a novel strategy for treatment of UC cells by GMIP alone or in combination with MMC application. |
| doi_str_mv | 10.1002/jcb.26616 |
| format | Article |
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Ganoderma microsporum immunomodulatory protein (GMIP) showed anti‐ urothelial carcinoma (UC) cell proliferation effect and classical apoptotic phenomenon in a p53‐independent but p21‐mediated manner. GMIP showed synergistic effects with Mitomycin C (MMC) in killing UC cells. Our results delineate a novel strategy for treatment of UC cells by GMIP alone or in combination with MMC application.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.26616</identifier><identifier>PMID: 29240252</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Activation ; Adjuvants ; Apoptosis ; Autophagy ; Bladder ; Bladder cancer ; bladder urothelial carcinoma ; Caspase ; Caspase-3 ; Cell cycle ; Cell death ; Cell proliferation ; Chemotherapy ; Chloroquine ; Cyclin-dependent kinase inhibitor p21 ; Design modifications ; G1 phase ; Ganoderma ; ganoderma microsporum immunomodulatory protein ; Immunomodulation ; Immunotherapy ; Lung cancer ; Membrane potential ; Mitochondria ; Mitomycin C ; Nuclear transport ; p53 Protein ; Phagocytosis ; Poly(ADP-ribose) polymerase ; Proteins ; Synergistic effect ; Translocation ; Urinary bladder ; Urothelial carcinoma</subject><ispartof>Journal of cellular biochemistry, 2018-06, Vol.119 (6), p.4592-4606</ispartof><rights>2017 Wiley Periodicals, Inc.</rights><rights>2018 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4196-5e6dd24d101e78a8b93cbbc512f3e15c9de970991397dec7c674c037d729059c3</citedby><cites>FETCH-LOGICAL-c4196-5e6dd24d101e78a8b93cbbc512f3e15c9de970991397dec7c674c037d729059c3</cites><orcidid>0000-0002-5346-3610</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcb.26616$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.26616$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,27922,27923,45572,45573</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29240252$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Sheng‐Yuan</creatorcontrib><creatorcontrib>Chien, Chih‐Cheng</creatorcontrib><creatorcontrib>Hseu, Ruey‐Shyang</creatorcontrib><creatorcontrib>Huang, Victoria Ying Jen</creatorcontrib><creatorcontrib>Chiang, Shang Ying</creatorcontrib><creatorcontrib>Huang, Chi‐Jung</creatorcontrib><creatorcontrib>Chen, Shao‐Kuan</creatorcontrib><creatorcontrib>Tsai, Ru‐Yin</creatorcontrib><creatorcontrib>Lin, Hsi‐Ting</creatorcontrib><creatorcontrib>Cheng, Yu‐Che</creatorcontrib><title>Ganoderma microsporum immunomodulatory protein induces apoptosis and potentiates mitomycin C‐induced apoptosis in urinary bladder urothelial carcinoma cells</title><title>Journal of cellular biochemistry</title><addtitle>J Cell Biochem</addtitle><description>Current chemotherapy and immunotherapy treatments followed by transurethral resection for urinary bladder urothelial carcinoma (UC) usually suffer from poor prognosis and high recurrence rate. Design and modification of current formulation with the novel adjuvants are needed. A recombinant protein derived from Ganoderma microsporum named as Ganoderma microsporum immunomodulatory protein (GMIP) was used to treat UC cells. We found GMIP elicits a dose‐dependent and time‐dependent anti‐UC cell proliferation effect, with a half‐maximal inhibition concentration (IC50) comparable to mitomycin C (MMC), a commonly used chemotherapy agent. After GMIP treatment, UC cells showed apoptotic phenomenon including cell cycle arrest in the G1 phase, elevated sub‐G1 population, mitochondrial membrane potential loss, up‐regulated p21 expression, p21 nuclear translocation, caspase activation, and PARP cleavage in a p53‐independent but p21‐mediated pathways. Unlike lung cancer cells, GMIP treated UC cells showed no autophagic scheme including Beclin‐1, an autophagy to apoptosis switch marker, was not cleaved by caspase 3 and slight LC3B‐II accumulation. Also, the classic autophagic inhibitor, chloroquine had no effect in GMIP‐mediated cell death made us conclude that GMIP induced apoptosis through caspase activation but not autophagy in UC cells. Additionally, GMIP showed synergistic effects with MMC in killing UC cells and thus decreased the concentration of MMC usage to reach the comparable apoptotic effects. Our results delineate novel strategies for treatment of UC by GMIP alone or in combination with MMC application and provide a promising therapeutic cocktail for better treatment of urinary bladder urothelial carcinoma.
Ganoderma microsporum immunomodulatory protein (GMIP) showed anti‐ urothelial carcinoma (UC) cell proliferation effect and classical apoptotic phenomenon in a p53‐independent but p21‐mediated manner. GMIP showed synergistic effects with Mitomycin C (MMC) in killing UC cells. Our results delineate a novel strategy for treatment of UC cells by GMIP alone or in combination with MMC application.</description><subject>Activation</subject><subject>Adjuvants</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Bladder</subject><subject>Bladder cancer</subject><subject>bladder urothelial carcinoma</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Cell cycle</subject><subject>Cell death</subject><subject>Cell proliferation</subject><subject>Chemotherapy</subject><subject>Chloroquine</subject><subject>Cyclin-dependent kinase inhibitor p21</subject><subject>Design modifications</subject><subject>G1 phase</subject><subject>Ganoderma</subject><subject>ganoderma microsporum immunomodulatory protein</subject><subject>Immunomodulation</subject><subject>Immunotherapy</subject><subject>Lung cancer</subject><subject>Membrane potential</subject><subject>Mitochondria</subject><subject>Mitomycin C</subject><subject>Nuclear transport</subject><subject>p53 Protein</subject><subject>Phagocytosis</subject><subject>Poly(ADP-ribose) polymerase</subject><subject>Proteins</subject><subject>Synergistic effect</subject><subject>Translocation</subject><subject>Urinary bladder</subject><subject>Urothelial carcinoma</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp1kT1OxDAQhS0EYpefggugSFQUWfyT2LiEFSwgJBqoI8f2Cq_iONiJ0HYcgRNwOE7CQADRUNnWfH4zbx5CBwTPCMb0ZKXrGeWc8A00JViKvOBFsYmmWDCcU0boBO2ktMIYS8noNppQSQtMSzpFbwvVBmOjV5l3OobUhTj4zHk_tMEHMzSqD3GddTH01rWZa82gbcpUF7o-JAe31mQdFNveqR4q3vXBrzWw8_eX15E3f3goDNG1CkTrRhnoDe_QP9rGqSbTKsLXAONo2zRpD20tVZPs_ve5ix4uL-7nV_nt3eJ6fnab64JInpeWG0MLQzCx4lSd1pLputYloUtmSamlsVKAecKkMFYLzUWhMRNGUIlLqdkuOhp1wefTYFNfrcIQW2hZUUwlLzkjJVDHI_W5qBTtsuqi8-CkIrj6TKKCJKqvJIA9_FYcam_NL_mzegBORuDZNXb9v1J1Mz8fJT8Ag8KYFQ</recordid><startdate>201806</startdate><enddate>201806</enddate><creator>Huang, Sheng‐Yuan</creator><creator>Chien, Chih‐Cheng</creator><creator>Hseu, Ruey‐Shyang</creator><creator>Huang, Victoria Ying Jen</creator><creator>Chiang, Shang Ying</creator><creator>Huang, Chi‐Jung</creator><creator>Chen, Shao‐Kuan</creator><creator>Tsai, Ru‐Yin</creator><creator>Lin, Hsi‐Ting</creator><creator>Cheng, Yu‐Che</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><orcidid>https://orcid.org/0000-0002-5346-3610</orcidid></search><sort><creationdate>201806</creationdate><title>Ganoderma microsporum immunomodulatory protein induces apoptosis and potentiates mitomycin C‐induced apoptosis in urinary bladder urothelial carcinoma cells</title><author>Huang, Sheng‐Yuan ; Chien, Chih‐Cheng ; Hseu, Ruey‐Shyang ; Huang, Victoria Ying Jen ; Chiang, Shang Ying ; Huang, Chi‐Jung ; Chen, Shao‐Kuan ; Tsai, Ru‐Yin ; Lin, Hsi‐Ting ; Cheng, Yu‐Che</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4196-5e6dd24d101e78a8b93cbbc512f3e15c9de970991397dec7c674c037d729059c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Activation</topic><topic>Adjuvants</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Bladder</topic><topic>Bladder cancer</topic><topic>bladder urothelial carcinoma</topic><topic>Caspase</topic><topic>Caspase-3</topic><topic>Cell cycle</topic><topic>Cell death</topic><topic>Cell proliferation</topic><topic>Chemotherapy</topic><topic>Chloroquine</topic><topic>Cyclin-dependent kinase inhibitor p21</topic><topic>Design modifications</topic><topic>G1 phase</topic><topic>Ganoderma</topic><topic>ganoderma microsporum immunomodulatory protein</topic><topic>Immunomodulation</topic><topic>Immunotherapy</topic><topic>Lung cancer</topic><topic>Membrane potential</topic><topic>Mitochondria</topic><topic>Mitomycin C</topic><topic>Nuclear transport</topic><topic>p53 Protein</topic><topic>Phagocytosis</topic><topic>Poly(ADP-ribose) polymerase</topic><topic>Proteins</topic><topic>Synergistic effect</topic><topic>Translocation</topic><topic>Urinary bladder</topic><topic>Urothelial carcinoma</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Sheng‐Yuan</creatorcontrib><creatorcontrib>Chien, Chih‐Cheng</creatorcontrib><creatorcontrib>Hseu, Ruey‐Shyang</creatorcontrib><creatorcontrib>Huang, Victoria Ying Jen</creatorcontrib><creatorcontrib>Chiang, Shang Ying</creatorcontrib><creatorcontrib>Huang, Chi‐Jung</creatorcontrib><creatorcontrib>Chen, Shao‐Kuan</creatorcontrib><creatorcontrib>Tsai, Ru‐Yin</creatorcontrib><creatorcontrib>Lin, Hsi‐Ting</creatorcontrib><creatorcontrib>Cheng, Yu‐Che</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Sheng‐Yuan</au><au>Chien, Chih‐Cheng</au><au>Hseu, Ruey‐Shyang</au><au>Huang, Victoria Ying Jen</au><au>Chiang, Shang Ying</au><au>Huang, Chi‐Jung</au><au>Chen, Shao‐Kuan</au><au>Tsai, Ru‐Yin</au><au>Lin, Hsi‐Ting</au><au>Cheng, Yu‐Che</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ganoderma microsporum immunomodulatory protein induces apoptosis and potentiates mitomycin C‐induced apoptosis in urinary bladder urothelial carcinoma cells</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J Cell Biochem</addtitle><date>2018-06</date><risdate>2018</risdate><volume>119</volume><issue>6</issue><spage>4592</spage><epage>4606</epage><pages>4592-4606</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>Current chemotherapy and immunotherapy treatments followed by transurethral resection for urinary bladder urothelial carcinoma (UC) usually suffer from poor prognosis and high recurrence rate. Design and modification of current formulation with the novel adjuvants are needed. A recombinant protein derived from Ganoderma microsporum named as Ganoderma microsporum immunomodulatory protein (GMIP) was used to treat UC cells. We found GMIP elicits a dose‐dependent and time‐dependent anti‐UC cell proliferation effect, with a half‐maximal inhibition concentration (IC50) comparable to mitomycin C (MMC), a commonly used chemotherapy agent. After GMIP treatment, UC cells showed apoptotic phenomenon including cell cycle arrest in the G1 phase, elevated sub‐G1 population, mitochondrial membrane potential loss, up‐regulated p21 expression, p21 nuclear translocation, caspase activation, and PARP cleavage in a p53‐independent but p21‐mediated pathways. Unlike lung cancer cells, GMIP treated UC cells showed no autophagic scheme including Beclin‐1, an autophagy to apoptosis switch marker, was not cleaved by caspase 3 and slight LC3B‐II accumulation. Also, the classic autophagic inhibitor, chloroquine had no effect in GMIP‐mediated cell death made us conclude that GMIP induced apoptosis through caspase activation but not autophagy in UC cells. Additionally, GMIP showed synergistic effects with MMC in killing UC cells and thus decreased the concentration of MMC usage to reach the comparable apoptotic effects. Our results delineate novel strategies for treatment of UC by GMIP alone or in combination with MMC application and provide a promising therapeutic cocktail for better treatment of urinary bladder urothelial carcinoma.
Ganoderma microsporum immunomodulatory protein (GMIP) showed anti‐ urothelial carcinoma (UC) cell proliferation effect and classical apoptotic phenomenon in a p53‐independent but p21‐mediated manner. GMIP showed synergistic effects with Mitomycin C (MMC) in killing UC cells. Our results delineate a novel strategy for treatment of UC cells by GMIP alone or in combination with MMC application.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>29240252</pmid><doi>10.1002/jcb.26616</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0002-5346-3610</orcidid></addata></record> |
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| subjects | Activation Adjuvants Apoptosis Autophagy Bladder Bladder cancer bladder urothelial carcinoma Caspase Caspase-3 Cell cycle Cell death Cell proliferation Chemotherapy Chloroquine Cyclin-dependent kinase inhibitor p21 Design modifications G1 phase Ganoderma ganoderma microsporum immunomodulatory protein Immunomodulation Immunotherapy Lung cancer Membrane potential Mitochondria Mitomycin C Nuclear transport p53 Protein Phagocytosis Poly(ADP-ribose) polymerase Proteins Synergistic effect Translocation Urinary bladder Urothelial carcinoma |
| title | Ganoderma microsporum immunomodulatory protein induces apoptosis and potentiates mitomycin C‐induced apoptosis in urinary bladder urothelial carcinoma cells |
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