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Background: Lung adenocarcinoma (LUAD) is a major type of lung cancer with poor prognosis and low 5-year survival rate, which urgently needs further investigation in order to elucidate its mechanisms completely and discover novel therapeutic targets. C1orf74 is a novel protein with unknown function either in normal cells or cancer cells. The aim of this study is to investigate the expression and function of C1orf74 in LUAD cells., Methods: The expression of C1orf74 in LUAD was analyzed using the LUAD datasets from public databases. The prognostic value of C1orf74 in LUAD was analyzed using Kaplan-Meier Plotter. C1orf74 expression in LUAD cell line A549, H1993 and HCC827 was silenced using small interfering RNA, and then the effects of C1orf74 knockdown on proliferation, migration and invasion of LUAD cells were detected by colony formation assay and Transwell assay, the role of C1orf74 in EGFR/AKT/mTORC1 signaling pathway was examined by Western blot, and the function of C1orf74 in cell cycle was detected by flow cytometry., Results: The results of LUAD clinical data showed that C1orf74 was upregulated in LUAD tissues, and its high expression was associated with poor prognosis. The results from cultured LUAD cells demonstrated that C1orf74 knockdown inhibited cell proliferation, migration and invasion, but induced cell cycle arrest and autophagy. Moreover, C1orf74 knockdown suppressed EGFR/AKT/mTORC1 signaling in LUAD cells. In conclusion, the present study revealed that C1orf74 is upregulated in LUAD tissues and plays an oncogenic role in LUAD, and that C1orf74 positively regulates cell proliferation and mobility through the EGFR/AKT/mTORC1 signaling pathway in LUAD cells., Competing Interests: The authors declare that they have no competing interests., (© 2022 Guo et al.)

DEP domain containing 1(DEPDC1) is involved in the tumorigenesis of a variety of cancers. But its role in tumorigenesis of lung adenocarcinoma (LUAD) is not fully understood. Here, we investigated the role and the underlying mechanisms of DEPDC1 in the development of LUAD. The expression and prognostic values of DEPDC1 in LUAD were analysed by using the data from public databases. Gene enrichment in TCGA LUAD was analysed using GSEA software with the pre-defined gene sets. Cell proliferation, migration and invasion of A549 cells were examined with colony formation, Transwell and wound healing assays. The function of DEPDC1 in autophagy and RAS-ERK1/2 signalling was determined with Western blot assay upon DEPDC1 knockdown and/or overexpression in A549, HCC827 and H1993 cells. The results demonstrated that DEPDC1 expression was up-regulated in LUAD tissues, and its high expression was correlated with unfavourable prognosis. The data also showed that DEPDC1 knockdown impaired proliferation, migration and invasion of A549 cells. Most notably, the results showed that DEPDC1 up-regulated RAS expression and thus enhanced ERK1/2 activity, through which DEPDC1 could inhibit autophagy. In conclusion, our study revealed that DEPDC1 is up-regulated in LUAD tissues and plays an oncogenic role in LUAD, and that DEPDC1 inhibits autophagy through the RAS-ERK1/2 signalling in A549, HCC827 and H1993 cells., (© 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)

This retraction relates to this paper Zhao F, Feng Y, Zhang X, Liu X, Li A. I Cancer Manag Res i . 2020;12:12769-12778. This includes the duplication of tumor images for Figure 5A with images for Figure 5A from Gao Z-Y, Yu F, Jia H-X, Ye Z, Yao S-J. ASPM predicts poor prognosis and regulates cell proliferation in bladder cancer. [Extracted from the article]

Background: The role of kinesin superfamily proteins (KIFs) has been reported in a variety of tumors and KIFs contributed to the proliferation of cancer cells. But few studies were focus on colon adenocarcinoma. Methods: Through bioinformatics analysis and immunohistochemistry (IHC) assays, the expression of KIF18B in colon adenocarcinoma tissues was determined. Stable KIF18B-depleted cell lines were constructed using lentivirus-mediated shRNA of KIF18B. Cell colony formation assay and CCK8 assay were performed to assess cell proliferation degree, and the expression level of KI67 and PCNA was used to indicate cell proliferation in vitro and verified using xenograft tumors in vivo. Results: KIF18B is highly expressed in colon adenocarcinoma tissues and has a negative correlation with the prognosis and tumor grade of colon adenocarcinoma. Interfering with KIF18B inhibits cell proliferation in vitro and in vivo. Conclusion: KIF18B can be used as a prognostic marker for colon adenocarcinoma and may be a therapeutic target for colon adenocarcinoma treatment. [ABSTRACT FROM AUTHOR]

The NICE-3 protein serves an oncogenic role in hepatocellular carcinoma, but its role in lung adenocarcinoma (LUAD) remains unknown. The aim of the present study was to investigate the potential role and underlying mechanisms of NICE-3 in LUAD. In the present study, NICE-3 expression in LUAD tissues and its association with patient prognosis were analyzed using datasets from The Cancer Genome Atlas and Gene Express Omnibus. After NICE-3-knockdown with small interfering RNA in LUAD cells, cell proliferation was measured by cell counting, cell cycle was examined by flow cytometry, cell invasion and migration were detected by Transwell assays and autophagic markers LC3 and p62, as well as phosphorylation of S6K and AKT, were determined by western blotting. The results of public database analysis demonstrated that compared with normal lung tissues, NICE-3 expression was increased in LUAD tissues, where high expression levels were associated with a poor prognosis. The results of in vitro experimentation in LUAD cells indicated that NICE-3-knockdown inhibited proliferation, cell cycle, migration and invasion, but enhanced autophagy. Notably, NICE-3-knockdown inhibited AKT/mTORC1 signaling. The present results suggested that NICE-3 may serve an oncogenic role in LUAD via the AKT/mTORC1 signaling pathway and may therefore be a potential therapeutic target for LUAD. [ABSTRACT FROM AUTHOR]

Melanocyte proliferating gene 1 (MYG1) is an exonuclease that participates in RNA processing and is required for normal mitochondrial function. However, its role in tumorigenesis remains unknown. The present study aimed to investigate the role of MYG1 and its underlying mechanisms in human lung adenocarcinoma (LUAD). The expression levels of MYG1 in tumor tissues of patients with LUAD were obtained from public cancer databases and analyzed using the UALCAN online software. The association between MYG1 expression levels and the prognosis of patients with LUAD was analyzed using the Kaplan-Meier plotter. In addition, the role of MYG1 in the LUAD A549 and H1993 cell lines was determined by knocking down MYG1 expression with a specific small interfering RNA or by overexpressing it with a MYG1-containing plasmid. The results demonstrated that MYG1 expression levels were upregulated in LUAD tissues compared with those in normal lung tissues from healthy subjects, and high MYG1 expression levels were associated with an unfavorable prognosis. MYG1 promoted the proliferation, migration and invasion of A549 and H1993 cells. In addition, MYG1 inhibited autophagy via the AMP-activated protein kinase/mTOR complex 1 signaling pathway. Collectively, the present results suggested that MYG1 may serve an oncogenic role in LUAD and may be a potential therapeutic target for LUAD. [ABSTRACT FROM AUTHOR]

Sperm-associated antigen 5 (SPAG5) is involved in the tumorigenesis of multiple cancer types. However, the role of SPAG5 during lung adenocarcinoma (LUAD) progression remains to be fully elucidated. In the present study, the expression of SPAG5 in tumor tissues of patients with LUAD from public cancer databases was analyzed using the online software Gene Expression Profiling Interactive Analysis and University of Alabama Cancer Database. The association of SPAG5 expression levels with the prognosis of patients with LUAD was analyzed using Kaplan-Meier Plotter. In addition, the role of SPAG5 in the LUAD cell line A549 was determined by knocking down its expression with specific small interfering RNA. The results demonstrated that SPAG5 expression was upregulated in LUAD tissues and its high expression was associated with unfavorable prognosis. Furthermore, in A549 cells, SPAG5 promoted proliferation, migration, invasion and autophagy, but inhibited apoptosis. The present results suggest that SPAG5 has an oncogenic role in LUAD and may be a potential prognostic predictor and therapeutic target for LUAD. [ABSTRACT FROM AUTHOR]