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| 1 | JUNB mediates oxaliplatin resistance via the MAPK signaling pathway in gastric cancer by chromatin accessibility and transcriptomic analysis显示文摘tients,and chemotherapy resistance is one of the main reasons for treatment failure.Thus,it is important to reveal the mechanism of oxaliplatin resistance and to seek effective intervention strategies to improve chemotherapy sensitivity,thereby improving the survival and prognosis of gastric cancer patients.To understand the molecular mechanisms of oxaliplatin resistance,we generate an oxaliplatin-resistant gastric cancer cell line and conduct assay for transposase-accessible chromatin sequencing(ATAC-seq)and RNA sequencing(RNA-seq)for both parental and oxaliplatin-resistant AGS cells.A total of 3232 genomic regions are identified to have higher accessibility in ox-aliplatin-resistant cells,and DNA-binding motif analysis identifies JUNB as the core transcription factor in the regulatory network.JUNB is overexpressed in oxaliplatin-resistant gastric cancer cells,and its upregulation is associated with poor prognosis in gastric cancer patients,which is validated by our tissue microarray data.Moreover,chromatin immunoprecipitation sequencing(ChIP-seq)analysis reveals that JUNB binds to the tran-scriptional start site of key genes involved in the MAPK signaling pathway.Knockdown of JUNB inhibits the MAPK signaling pathway and restores sensitivity to oxaliplatin.Combined treatment with the ERK inhibitor piperlongu-mine or MEK inhibitor trametinib effectively overcomes oxaliplatin resistance.This study provides evidence that JUNB mediates oxaliplatin resistance in gastric cancer by activating the MAPK pathway.The combination of MAPK inhibitors with oxaliplatin overcomes resistance to oxaliplatin,providing a promising treatment opportunity for oxaliplatin-resistant gastric cancer patients. | Suyao Li Yichou Wei Xun Sun Mengling Liu Mengxuan Zhu Yitao Yuan Jiayu Zhang Yu Dong Keshu Hu Sining Ma Xiuping Zhang Bei Xu Hesheng Jiang Lu Gan Tianshu Liu | 2023 | Acta Biochimica et Biophysica Sinica2023，55，11： | 0 |
| 2 | Tumor-derived exosomes:immune properties and clinical application in lung cancer显示文摘Lung cancer is the leading cause of cancer-related death worldwide.Despite advances in diagnosis and treatment of lung cancer,the overall survival remains poor.Evidence indicates that lung cancer development is a complex and dynamic process that involves interactions between tumor cells and their microenvironments,including immune cells.Exosomes are small extracellular vesicles secreted by most cell types;they contain functional molecules that allow intercellular communication.Tumor-derived exosomes(TEXs)carry both immunosuppressive and immunostimulatory mediators and may be involved in various immunomodulatory effects.TEXs,which partially mimic profiles of the parent cells,are a potential source of cancer biomarkers for prognosis,diagnosis,and prediction of response to therapy.In addition,TEXs may interfere with immunotherapies,but they also could be used as adjuvants and antigenic components in vaccines against lung cancer.In the context of lung cancer,identifying TEXs and understanding their contribution to tumorigenesis and the response to immunotherapies represents a challenging research area. | Jing Wu Suyao Li Pengfei Zhang | 2022 | Cancer Drug Resistance2022，5，1： | 0 |
| 3 | Negative correlation between acetyl-CoA acyltransferase 2 and cetuximab resistance in colorectal cancer显示文摘The emergence of anti-EGFR therapy has revolutionized the treatment of colorectal cancer(CRC).However,not all patients respond consistently well.Therefore,it is imperative to conduct further research to identify the molecular mechanisms underlying the development of cetuximab resistance in CRC.In this study,we find that the expressions of many metabolism-related genes are downregulated in cetuximab-resistant CRC cells compared to their sensitive counterparts.Specifically,acetyl-CoA acyltransferase 2(ACAA2),a key enzyme in fatty acid metabolism,is downregulated during the development of cetuximab resistance.Silencing of ACAA2 promotes proliferation and increases cetuximab tolerance in CRC cells,while overexpression of ACAA2 exerts the opposite effect.RTK-Kras signaling might contribute to the downregulation of ACAA2 expression in CRC,and ACAA2 predicts CRC prognosis in patients with Kras mutations.Collectively,our data suggest that modulating ACAA2 expression contributes to secondary cetuximab resistance in Kras wild-type CRC patients.ACAA2 expression is related to Kras mutation and demonstrates a prognostic role in CRC patients with Kras mutation.Thus,ACAA2 is a potential target in CRC with Kras mutation. | Yitao Yuan Xun Sun Mengling Liu Suyao Li Yu Dong Keshu Hu Jiayu Zhang Bei Xu Sining Ma Hesheng Jiang Pengcong Hou Yufu Lin Lu Gan Tianshu Liu | 2023 | Acta Biochimica et Biophysica Sinica2023，55，9： | 0 |
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