Berbamine targets cancer stem cells and reverses cabazitaxel resistance via inhibiting IGF2BP1 and p-STAT3 in prostate cancer
Cancer stem cells (CSCs) are a small subpopulation of tumor cells with the capability of self-renewal and drug resistance, leading to tumor progression and disease relapse. Our study aimed to investigate the antitumor effect of berbamine, extracted from berberis amurensis, on prostate CSCs. Sphere f...
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Veröffentlicht in: | The Prostate 2024-02, Vol.84 (2), p.131-147 |
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description | Cancer stem cells (CSCs) are a small subpopulation of tumor cells with the capability of self-renewal and drug resistance, leading to tumor progression and disease relapse. Our study aimed to investigate the antitumor effect of berbamine, extracted from berberis amurensis, on prostate CSCs.
Sphere formation was used to collect prostate CSCs. The viability, proliferation, invasion, migration, and apoptosis assays were used to evaluate the antitumor effect of berbamine on prostate CSCs. Prostate CSC markers were analyzed by flow cytometry and qRT-PCR. Small RNA sequencing analysis was conducted to analyse miRNAs. Exosomes were extracted using the ExoQuick-TC kit and verified by testing exosomal markers using western blot.
Berbamine targets prostate CSCs. Additionally, berbamine enhanced the antitumor effect of cabazitaxel, a second-line chemotherapeutic drug for advanced prostate cancer, and re-sensitized Cabazitaxel-resistant PCa cells (CabaR-DU145) to cabazitaxel by inhibiting ABCG2, CXCR4, IGF2BP1, and p-STAT3. Berbamine enhanced the expression of let-7 miRNA family and miR-26b and influenced the downstream targets IGF2BP1 and p-STAT3, respectively. Silencing CXCR4 and ABCG2 downregulated the expression of IGF2BP1 and p-STAT3, respectively. Importantly, berbamine enhanced also levels of exosomal let-7 family and miR-26b, suggesting that berbamine possibly influences the expression of let-7 family and miR-26b through exosome delivery. Exosomes derived from berbamine-treated CabaR-DU145 cells re-sensitized the cells to cabazitaxel.
Berbamine enhanced the toxic activity of cabazitaxel and reversed cabazitaxel resistance potentially through CXCR4/exosomal let-7/IGF2BP1 and ABCG2/exosomal miR-26b/p-STAT3 axes. |
doi_str_mv | 10.1002/pros.24632 |
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Sphere formation was used to collect prostate CSCs. The viability, proliferation, invasion, migration, and apoptosis assays were used to evaluate the antitumor effect of berbamine on prostate CSCs. Prostate CSC markers were analyzed by flow cytometry and qRT-PCR. Small RNA sequencing analysis was conducted to analyse miRNAs. Exosomes were extracted using the ExoQuick-TC kit and verified by testing exosomal markers using western blot.
Berbamine targets prostate CSCs. Additionally, berbamine enhanced the antitumor effect of cabazitaxel, a second-line chemotherapeutic drug for advanced prostate cancer, and re-sensitized Cabazitaxel-resistant PCa cells (CabaR-DU145) to cabazitaxel by inhibiting ABCG2, CXCR4, IGF2BP1, and p-STAT3. Berbamine enhanced the expression of let-7 miRNA family and miR-26b and influenced the downstream targets IGF2BP1 and p-STAT3, respectively. Silencing CXCR4 and ABCG2 downregulated the expression of IGF2BP1 and p-STAT3, respectively. Importantly, berbamine enhanced also levels of exosomal let-7 family and miR-26b, suggesting that berbamine possibly influences the expression of let-7 family and miR-26b through exosome delivery. Exosomes derived from berbamine-treated CabaR-DU145 cells re-sensitized the cells to cabazitaxel.
Berbamine enhanced the toxic activity of cabazitaxel and reversed cabazitaxel resistance potentially through CXCR4/exosomal let-7/IGF2BP1 and ABCG2/exosomal miR-26b/p-STAT3 axes.</description><identifier>ISSN: 0270-4137</identifier><identifier>EISSN: 1097-0045</identifier><identifier>DOI: 10.1002/pros.24632</identifier><identifier>PMID: 37828768</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Antitumor activity ; Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; CXCR4 protein ; Drug resistance ; Exosomes ; Exosomes - metabolism ; Flow cytometry ; Humans ; Male ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Neoplasm Recurrence, Local - pathology ; Neoplastic Stem Cells - metabolism ; Prostate cancer ; Prostatic Neoplasms - drug therapy ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - metabolism ; Sequence analysis ; Stat3 protein ; STAT3 Transcription Factor - metabolism ; Stem cells ; Tumor cells ; Tumors</subject><ispartof>The Prostate, 2024-02, Vol.84 (2), p.131-147</ispartof><rights>2023 The Authors. The Prostate published by Wiley Periodicals LLC.</rights><rights>2023. This article is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c310t-abf412d94b4badb0f0421326c1d48143c5aa350480d75e86d5cead5052dd9fc63</cites><orcidid>0000-0001-8296-2059</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37828768$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Lili</creatorcontrib><creatorcontrib>Lyu, Chen</creatorcontrib><creatorcontrib>Stadlbauer, Birgit</creatorcontrib><creatorcontrib>Buchner, Alexander</creatorcontrib><creatorcontrib>Nößner, Elfriede</creatorcontrib><creatorcontrib>Pohla, Heike</creatorcontrib><title>Berbamine targets cancer stem cells and reverses cabazitaxel resistance via inhibiting IGF2BP1 and p-STAT3 in prostate cancer</title><title>The Prostate</title><addtitle>Prostate</addtitle><description>Cancer stem cells (CSCs) are a small subpopulation of tumor cells with the capability of self-renewal and drug resistance, leading to tumor progression and disease relapse. Our study aimed to investigate the antitumor effect of berbamine, extracted from berberis amurensis, on prostate CSCs.
Sphere formation was used to collect prostate CSCs. The viability, proliferation, invasion, migration, and apoptosis assays were used to evaluate the antitumor effect of berbamine on prostate CSCs. Prostate CSC markers were analyzed by flow cytometry and qRT-PCR. Small RNA sequencing analysis was conducted to analyse miRNAs. Exosomes were extracted using the ExoQuick-TC kit and verified by testing exosomal markers using western blot.
Berbamine targets prostate CSCs. Additionally, berbamine enhanced the antitumor effect of cabazitaxel, a second-line chemotherapeutic drug for advanced prostate cancer, and re-sensitized Cabazitaxel-resistant PCa cells (CabaR-DU145) to cabazitaxel by inhibiting ABCG2, CXCR4, IGF2BP1, and p-STAT3. Berbamine enhanced the expression of let-7 miRNA family and miR-26b and influenced the downstream targets IGF2BP1 and p-STAT3, respectively. Silencing CXCR4 and ABCG2 downregulated the expression of IGF2BP1 and p-STAT3, respectively. Importantly, berbamine enhanced also levels of exosomal let-7 family and miR-26b, suggesting that berbamine possibly influences the expression of let-7 family and miR-26b through exosome delivery. Exosomes derived from berbamine-treated CabaR-DU145 cells re-sensitized the cells to cabazitaxel.
Berbamine enhanced the toxic activity of cabazitaxel and reversed cabazitaxel resistance potentially through CXCR4/exosomal let-7/IGF2BP1 and ABCG2/exosomal miR-26b/p-STAT3 axes.</description><subject>Antitumor activity</subject><subject>Apoptosis</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>CXCR4 protein</subject><subject>Drug resistance</subject><subject>Exosomes</subject><subject>Exosomes - metabolism</subject><subject>Flow cytometry</subject><subject>Humans</subject><subject>Male</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Neoplasm Recurrence, Local - pathology</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Prostate cancer</subject><subject>Prostatic Neoplasms - drug therapy</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Sequence analysis</subject><subject>Stat3 protein</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Stem cells</subject><subject>Tumor cells</subject><subject>Tumors</subject><issn>0270-4137</issn><issn>1097-0045</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkU1LAzEQhoMotlYv_gAJeBFhdfKxX0ctWgVBwXpessmspnS3NUlFBf-7WVs9eBqYeebjnZeQQwZnDICfL93Cn3GZCb5FhgzKPAGQ6TYZAs8hkUzkA7Ln_Qwg4sB3yUDkBS_yrBiSr0t0tWpthzQo94zBU606jY76gC3VOJ97qjpDHb6h89iXa_Vpg3rHeUx660PP0zerqO1ebG2D7Z7p7eSaXz6wn9Zl8ji9mIpYpv2pQQXcLNknO42aezzYxBF5ur6ajm-Su_vJ7fjiLtGCQUhU3UjGTSlrWStTQwOSM8EzzYwsmBQ6VUqkIAsweYpFZlKNyqSQcmPKRmdiRE7Wc-P-1xX6ULXW99pUh4uVr-IzclHkZckievwPnS1WrovXVbwEIQSILI3U6ZrSUZB32FRLZ1vlPioGVW9K1SutfkyJ8NFm5Kpu0fyhvy6Ibzsjh88</recordid><startdate>202402</startdate><enddate>202402</enddate><creator>Wang, Lili</creator><creator>Lyu, Chen</creator><creator>Stadlbauer, Birgit</creator><creator>Buchner, Alexander</creator><creator>Nößner, Elfriede</creator><creator>Pohla, Heike</creator><general>Wiley Subscription Services, Inc</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>7T5</scope><scope>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8296-2059</orcidid></search><sort><creationdate>202402</creationdate><title>Berbamine targets cancer stem cells and reverses cabazitaxel resistance via inhibiting IGF2BP1 and p-STAT3 in prostate cancer</title><author>Wang, Lili ; Lyu, Chen ; Stadlbauer, Birgit ; Buchner, Alexander ; Nößner, Elfriede ; Pohla, Heike</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c310t-abf412d94b4badb0f0421326c1d48143c5aa350480d75e86d5cead5052dd9fc63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Antitumor activity</topic><topic>Apoptosis</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>CXCR4 protein</topic><topic>Drug resistance</topic><topic>Exosomes</topic><topic>Exosomes - metabolism</topic><topic>Flow cytometry</topic><topic>Humans</topic><topic>Male</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Neoplasm Recurrence, Local - pathology</topic><topic>Neoplastic Stem Cells - metabolism</topic><topic>Prostate cancer</topic><topic>Prostatic Neoplasms - drug therapy</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Sequence analysis</topic><topic>Stat3 protein</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>Stem cells</topic><topic>Tumor cells</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Lili</creatorcontrib><creatorcontrib>Lyu, Chen</creatorcontrib><creatorcontrib>Stadlbauer, Birgit</creatorcontrib><creatorcontrib>Buchner, Alexander</creatorcontrib><creatorcontrib>Nößner, Elfriede</creatorcontrib><creatorcontrib>Pohla, Heike</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Prostate</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Lili</au><au>Lyu, Chen</au><au>Stadlbauer, Birgit</au><au>Buchner, Alexander</au><au>Nößner, Elfriede</au><au>Pohla, Heike</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Berbamine targets cancer stem cells and reverses cabazitaxel resistance via inhibiting IGF2BP1 and p-STAT3 in prostate cancer</atitle><jtitle>The Prostate</jtitle><addtitle>Prostate</addtitle><date>2024-02</date><risdate>2024</risdate><volume>84</volume><issue>2</issue><spage>131</spage><epage>147</epage><pages>131-147</pages><issn>0270-4137</issn><eissn>1097-0045</eissn><abstract>Cancer stem cells (CSCs) are a small subpopulation of tumor cells with the capability of self-renewal and drug resistance, leading to tumor progression and disease relapse. Our study aimed to investigate the antitumor effect of berbamine, extracted from berberis amurensis, on prostate CSCs.
Sphere formation was used to collect prostate CSCs. The viability, proliferation, invasion, migration, and apoptosis assays were used to evaluate the antitumor effect of berbamine on prostate CSCs. Prostate CSC markers were analyzed by flow cytometry and qRT-PCR. Small RNA sequencing analysis was conducted to analyse miRNAs. Exosomes were extracted using the ExoQuick-TC kit and verified by testing exosomal markers using western blot.
Berbamine targets prostate CSCs. Additionally, berbamine enhanced the antitumor effect of cabazitaxel, a second-line chemotherapeutic drug for advanced prostate cancer, and re-sensitized Cabazitaxel-resistant PCa cells (CabaR-DU145) to cabazitaxel by inhibiting ABCG2, CXCR4, IGF2BP1, and p-STAT3. Berbamine enhanced the expression of let-7 miRNA family and miR-26b and influenced the downstream targets IGF2BP1 and p-STAT3, respectively. Silencing CXCR4 and ABCG2 downregulated the expression of IGF2BP1 and p-STAT3, respectively. Importantly, berbamine enhanced also levels of exosomal let-7 family and miR-26b, suggesting that berbamine possibly influences the expression of let-7 family and miR-26b through exosome delivery. Exosomes derived from berbamine-treated CabaR-DU145 cells re-sensitized the cells to cabazitaxel.
Berbamine enhanced the toxic activity of cabazitaxel and reversed cabazitaxel resistance potentially through CXCR4/exosomal let-7/IGF2BP1 and ABCG2/exosomal miR-26b/p-STAT3 axes.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>37828768</pmid><doi>10.1002/pros.24632</doi><tpages>17</tpages><orcidid>https://orcid.org/0000-0001-8296-2059</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Antitumor activity Apoptosis Cell Line, Tumor Cell Proliferation CXCR4 protein Drug resistance Exosomes Exosomes - metabolism Flow cytometry Humans Male MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miRNA Neoplasm Recurrence, Local - pathology Neoplastic Stem Cells - metabolism Prostate cancer Prostatic Neoplasms - drug therapy Prostatic Neoplasms - genetics Prostatic Neoplasms - metabolism Sequence analysis Stat3 protein STAT3 Transcription Factor - metabolism Stem cells Tumor cells Tumors |
title | Berbamine targets cancer stem cells and reverses cabazitaxel resistance via inhibiting IGF2BP1 and p-STAT3 in prostate cancer |
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