After that, we applied the proposed method on different stage stratums and the performance demonstrates that LSCDFS-MKL remains efficient in DFS prediction of lung SCC patients.
Moreover, we found that the prognostic function of the eight miRNAs (miR-375, miR-148a, miR-29b-1 and miR-584 for LUAD; miR-4746, miR-326, miR-93 and miR-671 for LUSC).
Kaplan-Meier survival analysis showed that high levels of MEOX1 were significantly associated with unfavorable survival in NSCLC patients, and MEOX1 nucleus staining had worse survival, than did patients with overall expression in lung squamous cell carcinoma patients.
The frequencies of IL‑17A, IL‑17B and IL‑17C mRNA upregulation in lung squamous cell carcinoma were lower than those in lung adenocarcinoma (2.7, 1.9 and 2.1%, respectively), whereas the frequencies of IL‑17D, IL‑25 and IL‑17F mRNA upregulation were higher in lung squamous cell carcinoma than those in lung adenocarcinoma (3, 6 and 6%, respectively).
Furthermore, we identified seven specific lncRNAs (ERVH48-1, HCG9, SEC62-AS1, AC022148.1, LINC00460, C5orf17, LINC00261) as potential prognostic factors after correlation analysis, and five of the seven lncRNAs (AC022148.1, HCG9, LINC00460, C5orf17, LINC00261) constructed a prognostic model of LUSC.
TRIM15 upregulation was related to poor prognoses in both LUSC (HR 1.353; 95%CI 1.023-1.789; p =0.034) and LUAD (HR 1.560; 95%CI 1.159-2.101; p =0.003).
The two primary classification models consisted of four miRNAs for lung cancer diagnosis and subtyping. hsa-miR-183 and hsa-miR-135b were used to distinguish lung tumors from normal samples taken from tissues adjacent to the tumor site, and hsa-miR-944 and hsa-miR-205 to further classify the tumors into LUAD and LUSC major subtypes.
RESULTS SUMO1P3 was significantly increased in LUSC and LUAD tissues compared with adjacent normal lung tissue and was significantly co-expressed with SUMO1.
Based on survival analysis, 22 prognosis-associated lncRNAs (including surfactant associated 1, pseudogene (SFTA1P), long intergenic non-protein coding RNA 968 (LINC00968), GATA6 antisense RNA 1, (GATA6-AS1) TBX5 antisense RNA 1 (TBX5-AS1) and FEZF1 antisense RNA 1 (FEZF1-AS1)) in LUSC were selected from these DELs, and the associated abnormal expression levels were also verified in LUSC clinical samples.
A lncRNA-miRNA-mRNA ceRNA network including 121 DElncRNAs, 18 DEmiRNAs and 3 DEmRNAs was established, and univariate and multivariate Cox regression analysis of those 121 DElncRNAs showed a group of 3 DElncRNAs (<i>TTTY16</i>, <i>POU6F2-AS2</i> and <i>CACNA2D3-AS1</i>) had significantly prognostic value in OS of LUSC patients.
Complement and coagulation cascades, and ECM-receptor interaction might be the specific pathways for AC; smoking might have a closer relationship with SCC.</b>
Furthermore, we identified seven specific lncRNAs (ERVH48-1, HCG9, SEC62-AS1, AC022148.1, LINC00460, C5orf17, LINC00261) as potential prognostic factors after correlation analysis, and five of the seven lncRNAs (AC022148.1, HCG9, LINC00460, C5orf17, LINC00261) constructed a prognostic model of LUSC.
The frequencies of IL‑17A, IL‑17B and IL‑17C mRNA upregulation in lung squamous cell carcinoma were lower than those in lung adenocarcinoma (2.7, 1.9 and 2.1%, respectively), whereas the frequencies of IL‑17D, IL‑25 and IL‑17F mRNA upregulation were higher in lung squamous cell carcinoma than those in lung adenocarcinoma (3, 6 and 6%, respectively).
Functional assays revealed that ectopic expression of miR-144-5p and miR-144-3p significantly blocked the malignant abilities of LUSQ cells, eg, cancer cell proliferation, migration, and invasion.
CD271 knockdown in the LSCC cells completely suppressed their proliferation and tumor-formation capability, and increased their cell-cycle arrest in the G<sub>0</sub> phase.