Targeting tumor cell-to-macrophage communication by blocking Vtn-C1qbp interaction inhibits tumor progression via enhancing macrophage phagocytosis.

Cancer cells are capable of evading clearance by macrophages through overexpression of anti-phagocytic surface proteins known as "don't eat me" signals. Monoclonal antibodies that antagonize the "don't-eat-me" signaling in macrophages and tumor cells by targeting phagocytic checkpoints have shown therapeutic promises in several cancer types. However, studies on the responses to these drugs have revealed the existence of other unknown "don't eat me" signals.

Design, synthesis and biological evaluation of potent epidermal growth factor receptor tyrosine kinase (EGFR-TK) inhibitors against resistance mutation for lung cancer treatment.

In this study, we identified a newly synthesized compound 7o with potent inhibition on EGFR primary mutants (L858R, Del19) and drug-resistant mutant T790M with nanomolar IC values. 7o showed strong antiproliferative effects against EGFR mutant-driven non-small cell lung cancer (NSCLC) cells such as H1975, PC-9 and HCC827, over cells expressing EGFR. Molecular docking was performed to investigate the possible binding modes of 7o inside the binding site of EGFR and EGFR.

A Long Intergenic Non-coding RNA, LINC01426, Promotes Cancer Progression via AZGP1 and Predicts Poor Prognosis in Patients with LUAD.

Various long non-coding RNAs (lncRNAs) are closely associated with lung adenocarcinoma (LUAD), playing oncogenic or anti-oncogenic roles in tumorigenesis and progression. Herein, we report a novel lncRNA-long intergenic non-protein coding RNA 1426 (LINC01426)-that has not yet been characterized in LUAD. We note that LINC01426 expression was markedly upregulated in LUAD tissues, and that functional assays verified that LINC01426 knockdown markedly inhibited cell proliferation, migration, and invasion .