16 Papers
20 Citations
Kai Li is an academic researcher from Xi'an Jiaotong University. The author has contributed to research in topics: Medicine & Chemistry. The author has an hindex of 3, co-authored 11 publications.
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Papers
M6A associated TSUC7 inhibition contributed to Erlotinib resistance in lung adenocarcinoma through a notch signaling activation dependent way.
Kai Li,Zi-Yang Peng,Shan Gao,Qing-Shi Wang,Rui Wang,Xiang Li,Xiang Li,Guodong Xiao,Jing Zhang,Hong Ren,Shou-Ching Tang,Xin Sun +11 more
TL;DR: The specific gene features of candidates in association with resistance were explored, and found the miR-146a/Notch signaling was sustained highly activated in a m 6A dependent manner, and the m6A regulator of YTHDF2 suppressed TUSC7, and then contributed to the resistant features.
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Enhancement of TKI sensitivity in lung adenocarcinoma through m6A-dependent translational repression of Wnt signaling by circ-FBXW7
Kai Li,Zi-Yang Peng,Rui Wang,Xiang Li,Ning Du,Dapeng Liu,Jian Zhang,Yunfeng Zhang,Lei Ma,Shou Ching Tang,Hong Ren,Yi-Ping Yang,Xin Sun +12 more
TL;DR: In this paper , the authors used RNA Microarray and m6A Epi-Transcriptomic Microarray analyses to detect the polypeptide circRNA-AA, and its expression was confirmed through m 6A regulations.
An SETD1A/Wnt/β-catenin feedback loop promotes NSCLC development
TL;DR: The SET1/MLL family H3K4 methyltransferases are involved in the tumorigenesis of numerous cancers as mentioned in this paper, but the biological role and mechanism of SETD1A in non-small cell lung cancer (NSCLC) remain to be elucidated.
Stem signatures associated antibodies yield early diagnosis and precise prognosis predication of patients with non-small cell lung cancer.
Sisi Chen,Kai Li,Jie Wu,Zi-Yang Peng,Zhi-Dong Wang,Jichang Wang,Chongwen Xu,Cai-Lin Zhu,Bao-Cheng Li,Hong Ren,Shou-Ching Tang,Xin Sun +11 more
TL;DR: The detection regarding stem signatures associated antibodies could be used as effective tools in early NSCLC diagnosis, but not for localized screening of cancers, and their abnormal expression was in accordance with poorer survival.
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The interplay between ATF2 and NEAT1 contributes to lung adenocarcinoma progression.
TL;DR: ATF2 and NEAT1 form a positive feedback loop mediated by miR-26a-5p and coordinately contribute to LUAD progression, and rescue experiments showed that ATF2 exerted its oncogenic function in LUAD, at least, partly throughNEAT1 upregulation.