ArticleOncology reports2019
BH3 profiling discriminates the anti‑apoptotic status of 5‑fluorouracil‑resistant colon cancer cells.
Article in Oncology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Bcl‑xL‑specific BH3 mimetic A‑1331852 suppresses proliferation of fluorouracil‑resistant colorectal cancer cells by inducing apoptosis.Oncology reports · 2025Article
- Enhanced nuclear localization of phosphorylated MLKL predicts adverse events in patients with dilated cardiomyopathy.ESC heart failure · 2022Article
- KIFC3 Promotes Proliferation, Migration, and Invasion in Colorectal CancerFrontiers in genetics · 2022Article
- The manipulation of apoptosis for cancer therapy using BH3-mimetic drugs.Nature reviews. Cancer · 2022Review
- IL-1β enhances cell viability and decreases 5-FU sensitivity in novel colon cancer cell lines derived from African American patients.Frontiers in oncology · 2022Article
- Recent Updates on Mechanisms of Resistance to 5-Fluorouracil and Reversal Strategies in Colon Cancer Treatment.Biology · 2021Review
- BH3 Mimetic Sensitivity of Colorectal Cancer Cell Lines in Correlation with Molecular Features Identifies Predictors of Response.International journal of molecular sciences · 2021Article
- Acanthopanax senticosus Harms extract causes G0/G1 cell cycle arrest and autophagy via inhibition of Rubicon in human liver cancer cells.Oncology reports · 2021Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
5‑Fluorouracil (5‑FU) is a cytotoxic anticancer drug commonly used for patients with advanced colon cancer. This drug effectively reduces the size of tumors to a certain degree; however, cancer cells can gradually acquire resistance, resulting in disease progression. To identify the mechanism of 5‑FU resistance, we established three 5‑FU‑resistant colon cancer cell lines and analyzed both apoptosis‑related protein expression levels and BH3 profiling. These 5‑FU‑resistant colon cancer cell lines acquired apoptotic resistance to 5‑FU. Although apoptosis‑related protein expression levels were altered in each 5‑FU‑resistant colon cancer cell line variably, BH3 profiling indicated BCLXL dependence in 5‑FU‑resistant HT‑29 cells only. Functional BCLXL inhibition in 5‑FU‑resistant HT‑29 cells not only sensitized the cells to apoptosis but also overcame 5‑FU resistance. The apoptotic BIM protein was preferentially sequestered, thereby resulting in acquired dependence on BCLXL for survival. Additionally, in vivo models showed that BCLXL inhibition controlled tumor progression. These results indicate that BH3 profiling facilitates the identification of the functional role of anti‑apoptotic proteins during drug resistance and has clinical implications for colon cancer in targeting specific proteins such as BCLXL.
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Registered trials
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