Article in The FEBS journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
2 · The registry
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
9 authors.
Yue LiJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases and College of Pharmaceutical Sciences, The Fourth Affiliated Hospital of Soochow University, Jiangsu Province Engineering Research Center of Precision Diagnostics and Therapeutics Development, Jiangsu Key Laboratory of Preventive and Translational Medicine for Major Chronic Non-communicable Diseases, Suzhou Key Laboratory of Drug Research for Prevention and Treatment of Hyperlipidemic Diseases, Soochow University, China.
Chengpiao LuJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases and College of Pharmaceutical Sciences, The Fourth Affiliated Hospital of Soochow University, Jiangsu Province Engineering Research Center of Precision Diagnostics and Therapeutics Development, Jiangsu Key Laboratory of Preventive and Translational Medicine for Major Chronic Non-communicable Diseases, Suzhou Key Laboratory of Drug Research for Prevention and Treatment of Hyperlipidemic Diseases, Soochow University, China.
Jiaqi LuJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases and College of Pharmaceutical Sciences, The Fourth Affiliated Hospital of Soochow University, Jiangsu Province Engineering Research Center of Precision Diagnostics and Therapeutics Development, Jiangsu Key Laboratory of Preventive and Translational Medicine for Major Chronic Non-communicable Diseases, Suzhou Key Laboratory of Drug Research for Prevention and Treatment of Hyperlipidemic Diseases, Soochow University, China.
Honglv JiangJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases and College of Pharmaceutical Sciences, The Fourth Affiliated Hospital of Soochow University, Jiangsu Province Engineering Research Center of Precision Diagnostics and Therapeutics Development, Jiangsu Key Laboratory of Preventive and Translational Medicine for Major Chronic Non-communicable Diseases, Suzhou Key Laboratory of Drug Research for Prevention and Treatment of Hyperlipidemic Diseases, Soochow University, China.
Dan LiJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases and College of Pharmaceutical Sciences, The Fourth Affiliated Hospital of Soochow University, Jiangsu Province Engineering Research Center of Precision Diagnostics and Therapeutics Development, Jiangsu Key Laboratory of Preventive and Translational Medicine for Major Chronic Non-communicable Diseases, Suzhou Key Laboratory of Drug Research for Prevention and Treatment of Hyperlipidemic Diseases, Soochow University, China.
Guoqiang XuJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases and College of Pharmaceutical Sciences, The Fourth Affiliated Hospital of Soochow University, Jiangsu Province Engineering Research Center of Precision Diagnostics and Therapeutics Development, Jiangsu Key Laboratory of Preventive and Translational Medicine for Major Chronic Non-communicable Diseases, Suzhou Key Laboratory of Drug Research for Prevention and Treatment of Hyperlipidemic Diseases, Soochow University, China.ORCID https://orcid.org/0000-0002-4753-4769
Xiaohui WangJiangsu Key Laboratory of Drug Discovery and Translational Research for Brain Diseases and College of Pharmaceutical Sciences, The Fourth Affiliated Hospital of Soochow University, Jiangsu Province Engineering Research Center of Precision Diagnostics and Therapeutics Development, Jiangsu Key Laboratory of Preventive and Translational Medicine for Major Chronic Non-communicable Diseases, Suzhou Key Laboratory of Drug Research for Prevention and Treatment of Hyperlipidemic Diseases, Soochow University, China.ORCID https://orcid.org/0009-0004-0450-1686
Jingjing MaDepartment of Pharmacy, The Fourth Affiliated Hospital of Soochow University, Suzhou Dushu Lake Hospital, Medical Center of Soochow University, China.ORCID https://orcid.org/0000-0001-6731-1266
Funding
National Natural Science Foundation of China 32171437Suzhou Science and Technology Development Project SZM2023006
6 · The paper itself
Abstract
The application of platinum-based chemotherapy is often limited by drug resistance, which involves multiple signalling pathways. Although the sulfonamide anticancer agent indisulam has been utilised as an adjuvant in combination with cisplatin, olaparib, and temozolomide in clinical trials, the mechanism by which indisulam modulates the sensitivity of gastric cancer cells to these drugs remains elusive. Here, flow cytometry, TUNEL, and CCK-8 assays demonstrated that indisulam induced apoptosis in gastric cancer cells and enhanced their sensitivity to cisplatin and oxaliplatin. Label-free quantitative proteomics identified FKBP8 as a previously undescribed downstream target of indisulam in gastric cancer cells. qPCR analysis of clinical samples revealed a strong correlation between the mRNA levels of FKBP8 and RBM39, and Kaplan-Meier plot analyses indicated that high expression of FKBP8 mRNA was associated with reduced survival time for gastric cancer patients. Mechanistically, indisulam attenuated FKBP8 transcription, and depletion of FKBP8 enhanced apoptosis and reduced colony formation in the presence of cisplatin and oxaliplatin, thereby improving the chemotherapeutic response of gastric cancer cells to these drugs. FKBP8 overexpression abrogated the effect of indisulam and cisplatin on apoptosis and cell proliferation. Experiments using a xenograft mouse model further demonstrated that the combination of indisulam and cisplatin significantly inhibited the growth of gastric cancer cells, reduced FKBP8 mRNA levels, and increased apoptosis. Taken together, this and previous studies suggest that indisulam can inhibit viability and migration, but promote apoptosis of gastric cancer cells through distinct downstream targets, suggesting that FKBP8 could be leveraged as a therapeutic target in combination with chemotherapy for gastric cancer.
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
The sulfonamide anticancer agent indisulam enhances the chemosensitivity of gastric cancer cells by targeting FKBP8. · full record | OpenQuestion