Transfer of healthy fibroblast-derived mitochondria to HeLa ρ0 and SAS ρ0 cells recovers the proliferation capabilities of these cancer cells under conventional culture medium, but increase their sensitivity to cisplatin-induced apoptotic death
Mitochondrial dysfunction is known to contribute to cancer initiation, progression, and chemo-and radio-resistance. However, the precise role of mitochondria in cancer is controversial. Hence, here we tried to further clarify the role of mitochondria in cancer by transferring healthy mitochondria to...
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| Veröffentlicht in: | Molecular biology reports 2020-06, Vol.47 (6), p.4401-4411 |
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| creator | Roushandeh, Amaneh Mohammadi Tomita, Kazuo Kuwahara, Yoshikazu Jahanian-Najafabadi, Ali Igarashi, Kento Roudkenar, Mehryar Habibi Sato, Tomoaki |
| description | Mitochondrial dysfunction is known to contribute to cancer initiation, progression, and chemo-and radio-resistance. However, the precise role of mitochondria in cancer is controversial. Hence, here we tried to further clarify the role of mitochondria in cancer by transferring healthy mitochondria to cancer cells, and also to cells with depleted mitochondrial DNA (ρ
0
). Healthy mitochondria were isolated from WI-38 cells and were transferred to HeLa, SAS, HeLa ρ
0
,
and SAS ρ
0
cells. Then, cell proliferation was verified. In addition, the cells were treated by different concentrations of cisplatin and assessed for apoptosis induction and quantifying the mRNA expression of apoptosis-related genes. Results revealed that incubation of the HeLa, SAS and HeLa ρ
0
cells with 5 µg/ml of the isolated mitochondria for 24 h significantly (p |
| doi_str_mv | 10.1007/s11033-020-05493-5 |
| format | Article |
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0
). Healthy mitochondria were isolated from WI-38 cells and were transferred to HeLa, SAS, HeLa ρ
0
,
and SAS ρ
0
cells. Then, cell proliferation was verified. In addition, the cells were treated by different concentrations of cisplatin and assessed for apoptosis induction and quantifying the mRNA expression of apoptosis-related genes. Results revealed that incubation of the HeLa, SAS and HeLa ρ
0
cells with 5 µg/ml of the isolated mitochondria for 24 h significantly (p < 0.001) increased cell proliferation compared to non-treated controls. Interestingly, the mitochondria transfer rescued the ρ
0
cells and made them capable of growing under conventional culture medium. However, the number of apoptotic cells was significantly higher in the HeLa ρ
0
cells that received the mitochondria (HeLa-Fibro-Mit) compared to the HeLa ρ
0
. Furthermore, the expression level of BCL-2 anti-apoptotic gene was down-regulated in both HeLa-Fibro-Mit and SAS-Fibro-Mit cell lines while the expression levels of the BAX, caspase8, caspase9, and AIF pro-apoptotic genes were upregulated. Our findings indicated that although the response of cancer cells to the mitochondria transfer is cancer-type dependent, but the introduction of normal exogenous mitochondria to some cancer cells might be considered as a potential novel therapeutic strategy.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-020-05493-5</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Animal Anatomy ; Animal Biochemistry ; Apoptosis ; Apoptosis-inducing factor ; Bcl-2 protein ; Biomedical and Life Sciences ; Cancer ; Cell culture ; Cell growth ; Cell proliferation ; Chemotherapy ; Cisplatin ; Culture media ; Gene expression ; genes ; Histology ; Life Sciences ; Mitochondria ; Mitochondrial DNA ; Morphology ; Original Article ; therapeutics</subject><ispartof>Molecular biology reports, 2020-06, Vol.47 (6), p.4401-4411</ispartof><rights>Springer Nature B.V. 2020</rights><rights>Springer Nature B.V. 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c315t-14dc3e82c4100c891bd0471996cbbe29837a921300455b9428d7e74f757fe7c93</citedby><cites>FETCH-LOGICAL-c315t-14dc3e82c4100c891bd0471996cbbe29837a921300455b9428d7e74f757fe7c93</cites><orcidid>0000-0001-8364-7245</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/s11033-020-05493-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11033-020-05493-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids></links><search><creatorcontrib>Roushandeh, Amaneh Mohammadi</creatorcontrib><creatorcontrib>Tomita, Kazuo</creatorcontrib><creatorcontrib>Kuwahara, Yoshikazu</creatorcontrib><creatorcontrib>Jahanian-Najafabadi, Ali</creatorcontrib><creatorcontrib>Igarashi, Kento</creatorcontrib><creatorcontrib>Roudkenar, Mehryar Habibi</creatorcontrib><creatorcontrib>Sato, Tomoaki</creatorcontrib><title>Transfer of healthy fibroblast-derived mitochondria to HeLa ρ0 and SAS ρ0 cells recovers the proliferation capabilities of these cancer cells under conventional culture medium, but increase their sensitivity to cisplatin-induced apoptotic death</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><description>Mitochondrial dysfunction is known to contribute to cancer initiation, progression, and chemo-and radio-resistance. However, the precise role of mitochondria in cancer is controversial. Hence, here we tried to further clarify the role of mitochondria in cancer by transferring healthy mitochondria to cancer cells, and also to cells with depleted mitochondrial DNA (ρ
0
). Healthy mitochondria were isolated from WI-38 cells and were transferred to HeLa, SAS, HeLa ρ
0
,
and SAS ρ
0
cells. Then, cell proliferation was verified. In addition, the cells were treated by different concentrations of cisplatin and assessed for apoptosis induction and quantifying the mRNA expression of apoptosis-related genes. Results revealed that incubation of the HeLa, SAS and HeLa ρ
0
cells with 5 µg/ml of the isolated mitochondria for 24 h significantly (p < 0.001) increased cell proliferation compared to non-treated controls. Interestingly, the mitochondria transfer rescued the ρ
0
cells and made them capable of growing under conventional culture medium. However, the number of apoptotic cells was significantly higher in the HeLa ρ
0
cells that received the mitochondria (HeLa-Fibro-Mit) compared to the HeLa ρ
0
. Furthermore, the expression level of BCL-2 anti-apoptotic gene was down-regulated in both HeLa-Fibro-Mit and SAS-Fibro-Mit cell lines while the expression levels of the BAX, caspase8, caspase9, and AIF pro-apoptotic genes were upregulated. Our findings indicated that although the response of cancer cells to the mitochondria transfer is cancer-type dependent, but the introduction of normal exogenous mitochondria to some cancer cells might be considered as a potential novel therapeutic strategy.</description><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Apoptosis</subject><subject>Apoptosis-inducing factor</subject><subject>Bcl-2 protein</subject><subject>Biomedical and Life Sciences</subject><subject>Cancer</subject><subject>Cell culture</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Chemotherapy</subject><subject>Cisplatin</subject><subject>Culture media</subject><subject>Gene expression</subject><subject>genes</subject><subject>Histology</subject><subject>Life Sciences</subject><subject>Mitochondria</subject><subject>Mitochondrial DNA</subject><subject>Morphology</subject><subject>Original Article</subject><subject>therapeutics</subject><issn>0301-4851</issn><issn>1573-4978</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNqFkkGP1SAUhRujic_RP-CKxI0LUSjwKMvJRB2Tl7iYcd1QuLVMeFCBvuQt_YXzb1xLpyaTuNAVN-Q7h8vJaZrXlLynhMgPmVLCGCYtwURwxbB40uyokAxzJbunzY4wQjHvBH3evMj5jhDCqRS75tdt0iGPkFAc0QTal-mMRjekOHidC7aQ3AksOroSzRSDTU6jEtE1HDS6_0mQDhbdXN48zAa8zyiBiSdIGZUJ0Jyid9VeFxcDMnrWg_OuOMjrg5XIUG-DqQts6iXYdY7hBGHVaI_M4suSAB3BuuX4Dg1LQS6YBLqKq4VLKEPI1fXkynndzrg8-_pkwC7YxdT99RznEoszyIIu08vm2ah9hld_zovm26ePt1fX-PD185erywM2jIqCKbeGQdcaXlM2naKDJVxSpfZmGKBVHZNatZTVNIUYFG87K0HyUQo5gjSKXTRvN9-aw48FcumPLq8f1QHikvtWCKqkUB39P8oJ7Ui3V_uKvvkLvYtLqlGthlJKzqtvpdqNMinmnGDs5-SOOp17Svq1Nf3Wmr62pn9oTb-K2CbKFQ7fIT1a_0P1G3usyxU</recordid><startdate>20200601</startdate><enddate>20200601</enddate><creator>Roushandeh, Amaneh Mohammadi</creator><creator>Tomita, Kazuo</creator><creator>Kuwahara, Yoshikazu</creator><creator>Jahanian-Najafabadi, Ali</creator><creator>Igarashi, Kento</creator><creator>Roudkenar, Mehryar Habibi</creator><creator>Sato, Tomoaki</creator><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7TM</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>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</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>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>7S9</scope><scope>L.6</scope><orcidid>https://orcid.org/0000-0001-8364-7245</orcidid></search><sort><creationdate>20200601</creationdate><title>Transfer of healthy fibroblast-derived mitochondria to HeLa ρ0 and SAS ρ0 cells recovers the proliferation capabilities of these cancer cells under conventional culture medium, but increase their sensitivity to cisplatin-induced apoptotic death</title><author>Roushandeh, Amaneh Mohammadi ; 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However, the precise role of mitochondria in cancer is controversial. Hence, here we tried to further clarify the role of mitochondria in cancer by transferring healthy mitochondria to cancer cells, and also to cells with depleted mitochondrial DNA (ρ
0
). Healthy mitochondria were isolated from WI-38 cells and were transferred to HeLa, SAS, HeLa ρ
0
,
and SAS ρ
0
cells. Then, cell proliferation was verified. In addition, the cells were treated by different concentrations of cisplatin and assessed for apoptosis induction and quantifying the mRNA expression of apoptosis-related genes. Results revealed that incubation of the HeLa, SAS and HeLa ρ
0
cells with 5 µg/ml of the isolated mitochondria for 24 h significantly (p < 0.001) increased cell proliferation compared to non-treated controls. Interestingly, the mitochondria transfer rescued the ρ
0
cells and made them capable of growing under conventional culture medium. However, the number of apoptotic cells was significantly higher in the HeLa ρ
0
cells that received the mitochondria (HeLa-Fibro-Mit) compared to the HeLa ρ
0
. Furthermore, the expression level of BCL-2 anti-apoptotic gene was down-regulated in both HeLa-Fibro-Mit and SAS-Fibro-Mit cell lines while the expression levels of the BAX, caspase8, caspase9, and AIF pro-apoptotic genes were upregulated. Our findings indicated that although the response of cancer cells to the mitochondria transfer is cancer-type dependent, but the introduction of normal exogenous mitochondria to some cancer cells might be considered as a potential novel therapeutic strategy.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><doi>10.1007/s11033-020-05493-5</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0001-8364-7245</orcidid></addata></record> |
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| ispartof | Molecular biology reports, 2020-06, Vol.47 (6), p.4401-4411 |
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| language | eng |
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| subjects | Animal Anatomy Animal Biochemistry Apoptosis Apoptosis-inducing factor Bcl-2 protein Biomedical and Life Sciences Cancer Cell culture Cell growth Cell proliferation Chemotherapy Cisplatin Culture media Gene expression genes Histology Life Sciences Mitochondria Mitochondrial DNA Morphology Original Article therapeutics |
| title | Transfer of healthy fibroblast-derived mitochondria to HeLa ρ0 and SAS ρ0 cells recovers the proliferation capabilities of these cancer cells under conventional culture medium, but increase their sensitivity to cisplatin-induced apoptotic death |
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