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Black seed oil inhibits the migration of triple‐negative breast cancer cells and regulates MMP‐9 expression

Indonesian Journal of Biotechnology · Vol. 30 No. 1 (2025) · hlm. 47–55

DOI
10.22146/ijbiotech.96177
ISSN
2089-2241, 0853-8654
Terbit
2025-03-29
Penerbit
Universitas Gadjah Mada
Bahasa
eng
Lisensi
creativecommons.org/licenses/by-sa/4.0

Abstrak

Black seed (Nigella sativa L.) is well known for its pharmacological properties, particularly its anticancer activity, with previous studies demonstrating its cytotoxic effects on several cell lines, such as A‐549, DLD‐1, MDA‐MB231, or HCT. This study aims to investigate the effects of black seed oil (BSO) on the migratory activity of 4T1 triple‐negative breast cancer (TNBC) cells, focusing on its bioactive properties. BSO was extracted via hydro‐distillation and analyzed for its phytochemical composition using gas chromatography–mass spectrometry (GC‐MS). The cytotoxicity of BSO and doxorubicin (Dox) was assessed using the MTT assay. The effects of BSO and Dox on cell migration and matrix metalloproteinase‐9 (MMP‐9) expression were evaluated using a scratch wound‐healing assay and gelatin zymography method respectively. Additionally, intracellular reactive oxygen species (ROS) levels were measured using 2’,7’‐dichlorofluorescin diacetate (DCFDA) staining. GC‐MS analysis identified p‐cymene as a major component of BSO, along with various other bioactive compounds. BSO exhibited low toxicity toward 4T1 cells, while its combination with Dox reduced cell viability in a dose‐dependent manner. Furthermore, BSO in combination with Dox inhibited cell migration and suppressed MMP‐9 expressions in 4T1 cells. BSO treatment also led to an increase in ROS levels. In conclusion, BSO exhibits potential anticancer properties by inhibiting cell migration and downregulating MMP‐9 expression, highlighting its possible therapeutic role in TNBC treatment.

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Ratna Asmah SusidartiAfiliasi tidak diketahui20
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Muthi’ IkawatiAfiliasi tidak diketahui13
Rohmad Yudi UtomoAfiliasi tidak diketahui12
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Retno MurwantiAfiliasi tidak diketahui4
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Larasati LarasatiIPB University4
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Sri HandayaniUniversity of Brawijaya3
Ummi Maryam ZulfinAfiliasi tidak diketahui3
Erlina RivantiAfiliasi tidak diketahui3
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Asri Mega PutriAfiliasi tidak diketahui2
Hilyatul FadliyahAfiliasi tidak diketahui2
Yonika Arum LarasatiAfiliasi tidak diketahui2
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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)
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	<dc:title xml:lang="en-US">Black seed oil inhibits the migration of triple‐negative breast cancer cells and regulates MMP‐9 expression</dc:title>
	<dc:creator>Lintangsari, Ghina</dc:creator>
	<dc:creator>Aliyah, Alma Nuril</dc:creator>
	<dc:creator>Maran, Gergorius Gena</dc:creator>
	<dc:creator>Hermawan, Adam</dc:creator>
	<dc:creator>Meiyanto, Edy</dc:creator>
	<dc:subject xml:lang="en-US">4T1; Migration; MMP‐9; Nigella sativa; Triple‐negative breast cancer</dc:subject>
	<dc:description xml:lang="en-US">Black seed (Nigella sativa L.) is well known for its pharmacological properties, particularly its anticancer activity, with previous studies demonstrating its cytotoxic effects on several cell lines, such as A‐549, DLD‐1, MDA‐MB231, or HCT. This study aims to investigate the effects of black seed oil (BSO) on the migratory activity of 4T1 triple‐negative breast cancer (TNBC) cells, focusing on its bioactive properties. BSO was extracted via hydro‐distillation and analyzed for its phytochemical composition using gas chromatography–mass spectrometry (GC‐MS). The cytotoxicity of BSO and doxorubicin (Dox) was assessed using the MTT assay. The effects of BSO and Dox on cell migration and matrix metalloproteinase‐9 (MMP‐9) expression were evaluated using a scratch wound‐healing assay and gelatin zymography method respectively. Additionally, intracellular reactive oxygen species (ROS) levels were measured using 2’,7’‐dichlorofluorescin diacetate (DCFDA) staining. GC‐MS analysis identified p‐cymene as a major component of BSO, along with various other bioactive compounds. BSO exhibited low toxicity toward 4T1 cells, while its combination with Dox reduced cell viability in a dose‐dependent manner. Furthermore, BSO in combination with Dox inhibited cell migration and suppressed MMP‐9 expressions in 4T1 cells. BSO treatment also led to an increase in ROS levels. In conclusion, BSO exhibits potential anticancer properties by inhibiting cell migration and downregulating MMP‐9 expression, highlighting its possible therapeutic role in TNBC treatment.</dc:description>
	<dc:publisher xml:lang="en-US">Universitas Gadjah Mada</dc:publisher>
	<dc:contributor xml:lang="en-US"></dc:contributor>
	<dc:date>2025-03-29</dc:date>
	<dc:type>info:eu-repo/semantics/article</dc:type>
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	<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/96177</dc:identifier>
	<dc:identifier>10.22146/ijbiotech.96177</dc:identifier>
	<dc:source xml:lang="en-US">Indonesian Journal of Biotechnology; Vol 30, No 1 (2025); 47–55</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/96177/41321</dc:relation>
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	<dc:relation>https://journal.ugm.ac.id/ijbiotech/article/downloadSuppFile/96177/32866</dc:relation>
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	<dc:relation>https://journal.ugm.ac.id/ijbiotech/article/downloadSuppFile/96177/32868</dc:relation>
	<dc:relation>https://journal.ugm.ac.id/ijbiotech/article/downloadSuppFile/96177/32869</dc:relation>
	<dc:relation>https://journal.ugm.ac.id/ijbiotech/article/downloadSuppFile/96177/32870</dc:relation>
	<dc:relation>https://journal.ugm.ac.id/ijbiotech/article/downloadSuppFile/96177/32871</dc:relation>
	<dc:relation>https://journal.ugm.ac.id/ijbiotech/article/downloadSuppFile/96177/32872</dc:relation>
	<dc:rights xml:lang="en-US">Copyright (c) 2025 The Author(s)</dc:rights>
	<dc:rights xml:lang="en-US">http://creativecommons.org/licenses/by-sa/4.0</dc:rights>
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