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Gynura procumbens Prevents Chemoresistance through Inhibition MDR1 Expression on MCF-7 Breast Cancer Cell Line and Sensitizes the Cells to Doxorubicin

Indonesian Journal of Biotechnology · Vol. 17 No. 1 (2012) · hlm. 51–60

DOI
10.22146/ijbiotech.15998
ISSN
2089-2241, 0853-8654
Terbit
2012-06-03
Penerbit
Universitas Gadjah Mada
Bahasa
eng
Lisensi
creativecommons.org/licenses/by-sa/4.0

Abstrak

The long-term exposure of doxorubicin (Dox) causes enhancement in MDR1 expression that leads tobreast cancer cell resistance. This protein become a serious problem in cancer treatment and also well-knownas negative prognostic factor in breast cancer malignancies. The new approach using natural chemopreventivesubstance was developed to inhibit this resistance progress. This study was aimed to investigate whether ethylacetate fraction of Gynura procumnens (FEG) can prevent chemoresistance through suppressing the MDR1 proteinexpression. MCF-7 cell was used as chemoresistance cell model. The MCF-7 cells were maintained with 100nM Dox-contained medium for five weeks. The chemoprevention effect of FEG was investigated by treatedMCF-7/Dox with sub-toxic concentration of FEG. The cytotoxic properties of MCF-7 cells were determinedusing MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide) assay. Immunofluorescenceand western blotting analysis was performed to detect the MDR1 expression. MCF-7/Dox cells need higherconcentration for inhibiting cell growth, were compared with MCF-7, shown by IC50value. The MDR1 proteinlevel elevated after Dox exposure in time dependent manner. The FEG treatment decreased MDR-1 proteinlevel with dose dependent manner. FEG in combination with DOX potentiates the DOX effect on breast cancercell growth inhibition. The FEG prevents the chemoresistance development in breast cancer cell line, MCF-7induced by Dox through inhibiting MDR1 expression. The additional of FEG enhances Dox effect on cell deathinduction. Thus, FEG could be developed as co-chemotherapy agent for reverse multidrug resistance

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  • Universitas Gadjah Mada
  • Nara Institute of Science and Technology
  • Indonesian Institute of Sciences
  • Muhammadiyah University Purwokerto
  • Kementerian Kesehatan Republik Indonesia
  • Atma Jaya University Yogyakarta
  • Tanjungpura University
  • Organisasi lain
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Rekan penulisOrganisasiArtikel bersama
Ratna Asmah SusidartiUniversitas Gadjah Mada17
Adam HermawanUniversitas Gadjah Mada17
Riris Istighfari JenieUniversitas Gadjah Mada15
Muthi IkawatiUniversitas Gadjah Mada11
Rohmad Yudi UtomoUniversitas Gadjah Mada8
Dyaningtyas Dewi Pamungkas PutriUniversitas Gadjah Mada7
Faaza Aulia RahmanUniversitas Gadjah Mada5
Sari HaryantiKementerian Kesehatan Republik Indonesia5
Dhania NovitasariUniversitas Gadjah Mada4
Retno MurwantiUniversitas Gadjah Mada4
Desty Restia RahmawatiUniversitas Gadjah Mada4
Sri HandayaniIndonesian Institute of Sciences3
Ummi Maryam ZulfinUniversitas Gadjah Mada3
Anindyajati AnindyajatiUniversitas Gadjah Mada3
Larasati LarasatiUniversitas Gadjah Mada3
Erlina RivantiUniversitas Gadjah Mada3
M. MurwantokoAfiliasi tidak diketahui2
Sendy JunediAtma Jaya University Yogyakarta2
Langkah SembiringUniversitas Gadjah Mada2
Suwijiyo PramonoUniversitas Gadjah Mada2
Zalinar UdinIndonesian Institute of Sciences2
Yogi ErtantoUniversitas Gadjah Mada2
Lailatul QodriaUniversitas Gadjah Mada2
Gergorius Gena MaranUniversitas Gadjah Mada2
Aulia Nur SeptianiUniversitas Gadjah Mada2
Sofa FaridaUniversitas Gadjah Mada2
Beni LestariUniversitas Gadjah Mada2
Asri Mega PutriUniversitas Gadjah Mada2
Hilyatul FadliyahUniversitas Gadjah Mada2
Indri KusharyantiTanjungpura University2
Yonika Arum LarasatiUniversitas Gadjah Mada2
Raditya Prima IstiajiUniversitas Gadjah Mada2
Ni Putu Linda LaksmianiUdayana University2
Nanda Resa PratamaUniversitas Gadjah Mada2
Yurista GilangUniversitas Gadjah Mada2
Nindya Budiana PutriUniversitas Gadjah Mada2

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Sumber metadata: OAI-PMH (metadata jurnal) https://jurnal.ugm.ac.id/ijbiotech/oai, pertama di-harvest 8 Nov 2026, terakhir terlihat 8 Nov 2026.
Metadata asli (oai_dc) 
<oai_dc:dc xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/  http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
	<dc:title xml:lang="en-US">Gynura procumbens Prevents Chemoresistance through Inhibition MDR1 Expression on MCF-7 Breast Cancer Cell Line and Sensitizes the Cells to Doxorubicin</dc:title>
	<dc:creator>Nurulita, Nunuk Aries</dc:creator>
	<dc:creator>Meiyanto, Edy</dc:creator>
	<dc:creator>Matsuda, Eishou</dc:creator>
	<dc:creator>Kawaichi, Masashi</dc:creator>
	<dc:subject xml:lang="en-US">Gynura procumbens; Chemoresistance; MDR1; MCF-7; MCF-7/Dox</dc:subject>
	<dc:description xml:lang="en-US">The long-term exposure of doxorubicin (Dox) causes enhancement in MDR1 expression that leads tobreast cancer cell resistance. This protein become a serious problem in cancer treatment and also well-knownas negative prognostic factor in breast cancer malignancies. The new approach using natural chemopreventivesubstance was developed to inhibit this resistance progress. This study was aimed to investigate whether ethylacetate fraction of Gynura procumnens (FEG) can prevent chemoresistance through suppressing the MDR1 proteinexpression. MCF-7 cell was used as chemoresistance cell model. The MCF-7 cells were maintained with 100nM Dox-contained medium for five weeks. The chemoprevention effect of FEG was investigated by treatedMCF-7/Dox with sub-toxic concentration of FEG. The cytotoxic properties of MCF-7 cells were determinedusing MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide) assay. Immunofluorescenceand western blotting analysis was performed to detect the MDR1 expression. MCF-7/Dox cells need higherconcentration for inhibiting cell growth, were compared with MCF-7, shown by IC50value. The MDR1 proteinlevel elevated after Dox exposure in time dependent manner. The FEG treatment decreased MDR-1 proteinlevel with dose dependent manner. FEG in combination with DOX potentiates the DOX effect on breast cancercell growth inhibition. The FEG prevents the chemoresistance development in breast cancer cell line, MCF-7induced by Dox through inhibiting MDR1 expression. The additional of FEG enhances Dox effect on cell deathinduction. Thus, FEG could be developed as co-chemotherapy agent for reverse multidrug resistance</dc:description>
	<dc:publisher xml:lang="en-US">Universitas Gadjah Mada</dc:publisher>
	<dc:contributor xml:lang="en-US"></dc:contributor>
	<dc:date>2012-06-03</dc:date>
	<dc:type>info:eu-repo/semantics/article</dc:type>
	<dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
	<dc:type xml:lang="en-US">Original Research Articles</dc:type>
	<dc:format>application/pdf</dc:format>
	<dc:identifier>https://journal.ugm.ac.id/ijbiotech/article/view/15998</dc:identifier>
	<dc:identifier>10.22146/ijbiotech.15998</dc:identifier>
	<dc:source xml:lang="en-US">Indonesian Journal of Biotechnology; Vol 17, No 1 (2012); 51-60</dc:source>
	<dc:source>2089-2241</dc:source>
	<dc:source>0853-8654</dc:source>
	<dc:language>eng</dc:language>
	<dc:relation>https://journal.ugm.ac.id/ijbiotech/article/view/15998/10554</dc:relation>
	<dc:rights xml:lang="en-US">Copyright (c) 2016 Nunuk Aries Nurulita, Edy Meiyanto, Eishou Matsuda, Masashi Kawaichi</dc:rights>
	<dc:rights xml:lang="en-US">http://creativecommons.org/licenses/by-sa/4.0</dc:rights>
</oai_dc:dc>