Identification of an autophagy-related 12-lncRNA signature and evaluation of NFYC-AS1 as a pro-cancer factor in lung adenocarcinoma

Abstract

Objective: To develop an autophagy-related lncRNA-based risk signature and corresponding nomogram to predict overall survival (OS) for LUAD patients and investigate the possible meaning of screened factors.Methods: Differentially expressed lncRNAs and autophagy genes were screened between normal and LUAD tumor samples from the TCGA LUAD dataset. Univariate and multivariate Cox regression analyses were performed to construct the lncRNA-based risk signature and nomogram incorporating clinical information. Then, the accuracy and sensitivity were confirmed by the AUC of ROC curves in both training and validation cohorts. qPCR, immunoblot, shRNA, and ectopic expression were used to verify the positive regulation of NFYC-AS1 on BIRC6. CCK-8, immunofluorescence, and flow cytometry were used to confirm the influence of NFYC-AS1 on cell proliferation, autophagy, and apoptosis via BIRC6.Results: A 12-lncRNA risk signature and a nomogram combining related clinical information were constructed. Furthermore, the abnormal increase of NFYC-AS1 may promote LUAD progression through the autophagy-related gene BIRC6.Conclusion: 12-lncRNA signature may function as a predictive marker for LUAD patients, and NFYC-AS1 along with BIRC6 may function as carcinogenic factors in a combinatorial manner.

A graphSAGE discovers synergistic combinations of Gefitinib, paclitaxel, and Icotinib for Lung adenocarcinoma management by targeting human genes and proteins: the RAIN protocol

“…The conclusion is a 12-lncRNA signature may function as a predictive marker for LUAD patients, and NFYC-AS1 along with BIRC6 may function as carcinogenic factors in a combinatorial manner. 97,98…”

“…The conclusion is a 12-lncRNA signature may function as a predictive marker for LUAD patients, and NFYC-AS1 along with BIRC6 may function as carcinogenic factors in a combinatorial manner. 97,98 Zavitsanou's published work in bioRxiv that suggests Mutation in KEAP1 within lung adenocarcinoma encourages evasion of the immune system and resistance to immunotherapy. The study establishes that tumor-intrinsic KEAP1 mutations contribute to immune evasion through suppression of dendritic cell and T cell responses, explaining the observed resistance to immunotherapy of KEAP1 mutant tumors.…”

The pancancer overexpressed NFYC Antisense 1 controls cell cycle mitotic progression through in cis and in trans modes of action

“…In contrast, the information on NFYC-AS1 is scanty. While it was shown upregulated in lung adenocarcinoma (LUAD), with its silencing able to induce cell death in LUAD cells via both apoptosis and autophagy [ 19 , 20 ], crucial aspects of its biology remain to be elucidated. Here, we provide the first comprehensive characterization of NFYC-AS1 expression pancancer, accompanied by a refined annotation of its transcript and an initial characterization of its cell cycle-regulated expression, role in supporting cell growth, and dual in cis /in trans action.…”