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        <datestamp>2026-09-14T11:46:57Z</datestamp>
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          <dc:title>Supplementary file 1_CMTM6/PD-L1-targeted AAV promotes anti-tumor immune responses and chemotherapy responsiveness.xls</dc:title>
          <dc:creator>Runqiu Chen (18240979)</dc:creator>
          <dc:creator>Xiaoyu Pang (16145279)</dc:creator>
          <dc:creator>Fanglin Li (6112280)</dc:creator>
          <dc:creator>Shanna Wu (3384905)</dc:creator>
          <dc:creator>Yiting Wang (169115)</dc:creator>
          <dc:creator>Xinhang Zheng (6630032)</dc:creator>
          <dc:creator>Yaqi Zhao (397321)</dc:creator>
          <dc:creator>Fengru Qiu (24880549)</dc:creator>
          <dc:creator>Liying Chen (4223026)</dc:creator>
          <dc:creator>Fengyu Du (9131929)</dc:creator>
          <dc:creator>Chen Chen (6544)</dc:creator>
          <dc:creator>Rong Zhang (44942)</dc:creator>
          <dc:creator>Zhiying Li (703571)</dc:creator>
          <dc:creator>Yiru Long (22177924)</dc:creator>
          <dc:creator>Likun Gong (172599)</dc:creator>
          <dc:creator>Meiqing Feng (447657)</dc:creator>
          <dc:subject>Genetic Immunology</dc:subject>
          <dc:subject>adeno-associated virus</dc:subject>
          <dc:subject>chemotherapy</dc:subject>
          <dc:subject>CMTM6</dc:subject>
          <dc:subject>immunotherapy</dc:subject>
          <dc:subject>PD-L1</dc:subject>
          <dc:description>&lt;p&gt;Chemotherapy is one of the important clinical treatments for malignant tumors, but primary or acquired chemotherapy resistance significantly limits patient benefits. Programmed death ligand 1 (PD-L1) has been reported to be regulated by chemotherapy and to contribute to chemotherapy resistance. However, as a novel regulatory molecule of PD-L1, the relationship between CKLF-like MARVEL transmembrane domain-containing protein 6 (CMTM6) and chemotherapy resistance remains understudied. Here, we found that tumor CMTM6 and PD-L1 were upregulated by chemotherapy in clinical cancer patients, in vitro human or mouse tumor models, and in vivo mouse tumor models. PI3K-mTOR was the potential mechanism underlying this effect. CMTM6 deficiency could still reduce chemotherapy-induced tumor PD-L1 expression. And CMTM6 could promote tumor cell resistance to chemotherapy-induced apoptosis and growth arrest, which may be associated with p53. In vivo, both tumor and host CMTM6 and PD-L1 could promote resistance to chemotherapy, and tumor and host CMTM6 knockout could promoted antitumor immune responses during chemotherapy. Moreover, we developed and evaluated the antitumor effects of CMTM6&amp;PD-L1-targeting adeno-associated virus (AAV), which effectively mobilized antitumor immunity and could be combined with chemotherapy. Our findings reveal that both tumor- and host-derived CMTM6 and PD-L1 are regulatory molecules of chemotherapy resistance and can serve as therapeutic targets for combination therapy with chemotherapy.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-14T11:46:57Z</dc:date>
          <dc:type>Dataset</dc:type>
          <dc:type>Dataset</dc:type>
          <dc:identifier>10.3389/fimmu.2026.1886034.s002</dc:identifier>
          <dc:relation>https://figshare.com/articles/dataset/Supplementary_file_1_CMTM6_PD-L1-targeted_AAV_promotes_anti-tumor_immune_responses_and_chemotherapy_responsiveness_xls/33734242</dc:relation>
          <dc:rights>CC BY 4.0</dc:rights>
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