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https://www.selleckchem.com/products/CP-690550.html HMGB1 immunoprecipitated NHEJ key factors in NPC cells and promoted DNA-binding activity of Ku70. Mutational analysis revealed that serine 155 of Ku70 was required for its direct interaction with HMGB1. HMGB1 was highly expressed in radio- and chemoresistant NPC cells. Deficiency of HMGB1 sensitized wild-type (WT) and resistant NPC cells to IR and cisplatin. Glycyrrhizin, which is HMGB1 inhibitor, impaired DNA binding of HMGB1 and exhibited excellent synergy with IR and cisplatin. Conclusion HMGB1 promotes NHEJ via interaction with Ku70 resulting in resistance to IR and cisplatin. Inhibition of HMGB1 by glycyrrhizin is a potential therapeutic regimen to treat cisplatin and IR resistant NPC patients.Anaplastic lymphoma kinase (ALK) fusion is present in approximately 2-7% of patients with lung adenocarcinoma. ALK fusion-positive patients can benefit from targeted therapy. We herein report a 53-year-old Chinese male patient diagnosed as lung adenocarcinoma with a smoking history. Next-generation sequencing was performed to detect somatic mutations of oncogenic drivers and tumor suppressor genes in plasma-derived circulating tumor DNA using an ultra-deep 160-gene panel. A novel HPCAL1-ALK fusion variant was identified in the patient responding to ALK inhibitor treatments, and the fusion variant was also confirmed by fluorescence in situ hybridization and immunohistochemical. Our study expands the mutational spectrum of ALK fusion variants and provides options for the precise treatment of such patients.Purpose LncRNA-UCA1 has been proven to facilitate the proliferation and metastasis of colon cancer. Whether metformin inhibits the progression of colon cancer by suppressing lncRNA-UCA1 remains unknown. In this research, we aimed to explore the role of Metformin playing in pathogenesis of colon cancer. Materials and methods Using qRT-PCR, we measured the expression of five tumor-promoting lncRNAs in SW480 and SW620 colon

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