ArticleOncology letters2018
ATPase inhibitory factor 1 inhibition improves the antitumor of YC-1 against hepatocellular carcinoma.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Peptides Targeting the IF1-ATP Synthase Complex Modulate the Permeability Transition Pore in Cancer HeLa Cells.International journal of molecular sciences · 2024Article
- The mitochondrial inhibitor IF1 binds to the ATP synthase OSCP subunit and protects cancer cells from apoptosis.Cell death & disease · 2023Article
- Synthetic strategy and structure-activity relationship (SAR) studies of 3-(5'-hydroxymethyl-2'-furyl)-1-benzyl indazole (YC-1, Lificiguat): a review.RSC advances · 2021Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
YC-1 is a synthetic compound, which serves as a hypoxia-inducible factor 1-α inhibitor or sensitizer to enhance the effect of chemotherapy. Previous studies have revealed the anti-cancer effects of YC-1 in various types of cancer, including hepatocellular carcinoma (HCC). ATPase inhibitory factor 1 (IF1) is upregulated in a number of human carcinomas and regulates mitochondrial bioenergetics and structure. However, whether IF1 is involved in the antitumor effects of YC-1 against HCC remains unclear. The present study examined the function of IF1 in HCC and its potential role in YC-1 effects within HCC cells. MTT, colony formation and Transwell assays revealed that IF1 overexpression promoted proliferation, colony formation and invasion of HCC cells, while IF1 downregulation had the opposite effects. Overexpression of IF1 reversed the inhibitory effects of YC-1 on Huh7 cell growth and invasion activities, while downregulation of IF1 increased the sensitivity of HCCLM3 cells to YC-1. YC-1 treatment of HCCLM3 and Huh7 cells reduced the levels of phosphorylated (p-) signal transducer and activator of transcription 3 (STAT3) and IF1, and increased the expression of E-cadherin. IF1 knockdown resulted in decreased p-STAT3 levels and increased E-cadherin expression, while IF1 overexpression increased p-STAT3 levels and reduced the expression of E-cadherin. The present study demonstrated that the inhibition of IF1 improves the antitumor effects of YC-1 in HCC cells. These findings support the clinical strategy of combining YC-1 and an IF1 inhibitor for the treatment of HCC.
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Registered trials
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