Effect and Mechanism of TFAM on Chemotherapy Resistance in Ovarian Cancer Cells Through Metabolic Reprogramming Regulation

ObjectiveTo investigate the role of mitochondrial transcription factor A (TFAM) in platinum-resistant ovarian cancer cells and its effects on metabolic reprogramming and sensitivity to platinum-based drugs MethodsThe mitochondrial function and metabolic characteristics of platinum-resistant ovarian...

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Main Authors: Lingling FAN, Reziwanguli·WUBULI, Linglan LU, Lili HAN
Format: Article
Language:zho
Published: Magazine House of Cancer Research on Prevention and Treatment 2025-05-01
Series:Zhongliu Fangzhi Yanjiu
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Online Access:http://www.zlfzyj.com/cn/article/doi/10.3971/j.issn.1000-8578.2025.24.1072
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author Lingling FAN
Reziwanguli·WUBULI
Linglan LU
Lili HAN
author_facet Lingling FAN
Reziwanguli·WUBULI
Linglan LU
Lili HAN
author_sort Lingling FAN
collection DOAJ
description ObjectiveTo investigate the role of mitochondrial transcription factor A (TFAM) in platinum-resistant ovarian cancer cells and its effects on metabolic reprogramming and sensitivity to platinum-based drugs MethodsThe mitochondrial function and metabolic characteristics of platinum-resistant ovarian cancer cells were analyzed. A TFAM-overexpressing cell model was established to assess its effects on platinum sensitivity, mitochondrial function, and aerobic glycolysis; and glycolytic enzyme and drug-resistant protein expression were analyzed. ResultsPlatinum-resistant ovarian cancer cells exhibited considerable mitochondrial dysfunction (reduced oxygen consumption rate) and enhanced aerobic glycolysis (increased extracellular acidification rate, glucose uptake, and lactate production). TFAM was downregulated in resistant cells. Meanwhile, TFAM overexpression significantly enhanced platinum sensitivity (P<0.01), restored mitochondrial function, and inhibited aerobic glycolysis. The expression levels of glycolytic enzymes and drug-resistant proteins were also downregulated (P<0.05). ConclusionTFAM downregulation is associated with suppressed oxidative phosphorylation and enhanced aerobic glycolysis in platinum-resistant ovarian cancer cells. TFAM overexpression can restore cellular dependence on oxidative phosphorylation and increase platinum sensitivity, suggesting that TFAM is a potential therapeutic target for reversing platinum resistance.
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publisher Magazine House of Cancer Research on Prevention and Treatment
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series Zhongliu Fangzhi Yanjiu
spelling doaj-art-4c1edc19b361465d8da801063b4bbf6a2025-08-20T03:21:34ZzhoMagazine House of Cancer Research on Prevention and TreatmentZhongliu Fangzhi Yanjiu1000-85782025-05-0152537438110.3971/j.issn.1000-8578.2025.24.107220241072Effect and Mechanism of TFAM on Chemotherapy Resistance in Ovarian Cancer Cells Through Metabolic Reprogramming RegulationLingling FAN0Reziwanguli·WUBULI1Linglan LU2Lili HAN3Department of Gynecology, People’s Hospital of Xinjiang Uygur Autonomous Region, Urumqi 830002, ChinaDepartment of Gynecology, People’s Hospital of Xinjiang Uygur Autonomous Region, Urumqi 830002, ChinaDepartment of Gynecology, People’s Hospital of Xinjiang Uygur Autonomous Region, Urumqi 830002, ChinaDepartment of Gynecology, People’s Hospital of Xinjiang Uygur Autonomous Region, Urumqi 830002, ChinaObjectiveTo investigate the role of mitochondrial transcription factor A (TFAM) in platinum-resistant ovarian cancer cells and its effects on metabolic reprogramming and sensitivity to platinum-based drugs MethodsThe mitochondrial function and metabolic characteristics of platinum-resistant ovarian cancer cells were analyzed. A TFAM-overexpressing cell model was established to assess its effects on platinum sensitivity, mitochondrial function, and aerobic glycolysis; and glycolytic enzyme and drug-resistant protein expression were analyzed. ResultsPlatinum-resistant ovarian cancer cells exhibited considerable mitochondrial dysfunction (reduced oxygen consumption rate) and enhanced aerobic glycolysis (increased extracellular acidification rate, glucose uptake, and lactate production). TFAM was downregulated in resistant cells. Meanwhile, TFAM overexpression significantly enhanced platinum sensitivity (P<0.01), restored mitochondrial function, and inhibited aerobic glycolysis. The expression levels of glycolytic enzymes and drug-resistant proteins were also downregulated (P<0.05). ConclusionTFAM downregulation is associated with suppressed oxidative phosphorylation and enhanced aerobic glycolysis in platinum-resistant ovarian cancer cells. TFAM overexpression can restore cellular dependence on oxidative phosphorylation and increase platinum sensitivity, suggesting that TFAM is a potential therapeutic target for reversing platinum resistance.http://www.zlfzyj.com/cn/article/doi/10.3971/j.issn.1000-8578.2025.24.1072mitochondrial transcription factor aaerobic glycolysisoxidative phosphorylationovarian cancerchemotherapy resistance
spellingShingle Lingling FAN
Reziwanguli·WUBULI
Linglan LU
Lili HAN
Effect and Mechanism of TFAM on Chemotherapy Resistance in Ovarian Cancer Cells Through Metabolic Reprogramming Regulation
Zhongliu Fangzhi Yanjiu
mitochondrial transcription factor a
aerobic glycolysis
oxidative phosphorylation
ovarian cancer
chemotherapy resistance
title Effect and Mechanism of TFAM on Chemotherapy Resistance in Ovarian Cancer Cells Through Metabolic Reprogramming Regulation
title_full Effect and Mechanism of TFAM on Chemotherapy Resistance in Ovarian Cancer Cells Through Metabolic Reprogramming Regulation
title_fullStr Effect and Mechanism of TFAM on Chemotherapy Resistance in Ovarian Cancer Cells Through Metabolic Reprogramming Regulation
title_full_unstemmed Effect and Mechanism of TFAM on Chemotherapy Resistance in Ovarian Cancer Cells Through Metabolic Reprogramming Regulation
title_short Effect and Mechanism of TFAM on Chemotherapy Resistance in Ovarian Cancer Cells Through Metabolic Reprogramming Regulation
title_sort effect and mechanism of tfam on chemotherapy resistance in ovarian cancer cells through metabolic reprogramming regulation
topic mitochondrial transcription factor a
aerobic glycolysis
oxidative phosphorylation
ovarian cancer
chemotherapy resistance
url http://www.zlfzyj.com/cn/article/doi/10.3971/j.issn.1000-8578.2025.24.1072
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AT reziwanguliwubuli effectandmechanismoftfamonchemotherapyresistanceinovariancancercellsthroughmetabolicreprogrammingregulation
AT linglanlu effectandmechanismoftfamonchemotherapyresistanceinovariancancercellsthroughmetabolicreprogrammingregulation
AT lilihan effectandmechanismoftfamonchemotherapyresistanceinovariancancercellsthroughmetabolicreprogrammingregulation