<scp>DDA</scp>1, a novel oncogene, promotes lung cancer progression through regulation of cell cycle

Cheng, Lin; Yang, Qianmei; Li, Can; Dai, Lei; Yang, Yang; Wang, Qingnan; Ding, Yu; Zhang, Junfeng; Liu, Lei; Zhang, Shuang; Fan, Ping; Hu, Xun; Xiang, Rong; Yu, Dechao; Wei, Yuquan; Deng, Hongxin

doi:10.1111/jcmm.13084

Cited by 15 publications

(13 citation statements)

References 50 publications

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“…48 hours post transfection, the transfected H292 and A549 cells were collected and stained with PI for 30 mins. Then Cytomics FC500 flow cytometer (Beckman Coulter) was used to analyze the cell cycle of cells according to the fold of DNA as the previous study indicated [ 23 ]. Each experiment was performed in triplicate.…”

Section: Methodsmentioning

confidence: 99%

TIPE1 function as a prognosis predictor and negative regulator of lung cancer

et al. 2017

Oncotarget

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TIPE1 (tumor necrosis factor-α-induced protein 8-like 1 or TNFAIP8L1) belongs to the TIPE (TNFAIP8) family, which act as a regulator of cell death. However, the expression and biologic functions of TIPE1 in lung cancer are largely unknown. Here, we investigated the roles of TIPE1 in lung cancer. Evaluated by qRT-PCR and immunohistochemical staining, lower TIPE1 mRNA and protein expression was found in the lung tumor tissue, compared with adjacent non-tumor tissues, which positively correlated with tumor patient survival. Overexpression of TIPE1 by lentivirus system in TIPE1-downregulated lung cancer cells significantly diminished cell growth and colony formation, companied with proliferation inhibition, apoptosis induction and invasion inhibition. It was identified to be due to TIPE1-regulated Cyclin D1, Cyclin B1, caspase 8, Caspase3, MM2 and MMP9 expression. Consistently, using a homograft tumor model in Balb/c mice, we discovered that TIPE1 prevented the growth and tumor weight of murine lung cancer homografts. Our findings revealed the anti-tumor role of TIPE1 in lung cancer cells and TIPE1 might be a novel prognostic indicator for lung cancer patients.

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Section: Methodsmentioning

confidence: 99%

TIPE1 function as a prognosis predictor and negative regulator of lung cancer

et al. 2017

Oncotarget

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“…Since cancer is characterized by the deregulation of cell cycle activity that lead to aberrant cell proliferation [32][33], many authors have concluded that cancer can be regarded as a disease of the cell cycle [34]. Previous studies reported that many genes can regulate cell cycles to promote LC cell proliferations [35][36][37][38]. Disappointingly, there is no relevant study about the molecular mechanism of SYNJ2 in LUAD.…”

Section: Discussionmentioning

confidence: 99%

The Clinical Significance and Potential Molecular Mechanisms of Synaptojanin 2 in Lung Adenocarcinoma

Chen

et al. 2020

Preprint

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Background Lung adenocarcinoma (LUAD) is the main pathological type of pulmonary malignant tumors. Synaptojanin 2 (SYNJ2), a member of the synaptojanin family, is considered as an attractive underlying therapeutic target in several types of cancer. The purpose of the current research was to comprehensively investigate the molecular function and underlying mechanism of SYNJ2 in LUAD with the goal of providing a promising therapeutic target for LUAD. Methods We applied tissue microarrays, immunohistochemistry (IHC), high-throughput RNA sequencing (RNA-seq) data, and gene microarrays of public databases to comprehensively examine the protein level, mRNA expression, clinical significance, and prognosis value of SYNJ2 in LUAD. The standard mean difference (SMD) and summary receiver operating characteristic curves (SROC) were computed to evaluate the comprehensive expression value of SYNJ2 in LUAD. Kaplan-Meier survival curves were plotted to determine the overall survival of SYNJ2 with different expression levels in LUAD. Univariate and multivariate cox regression analyses were implemented to investigate the dependent prognostic ability of SYNJ2 expression and the clinically-relevant traits of LUAD. Moreover, SYNJ2 co-expressed genes were screened for Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) function analysis and protein–protein interactions (PPI) network construction. Results SYNJ2 overexpression in LUAD was confirmed by 2,299 LUAD samples and 1,387 non-tumor tissues obtained from tissue microarrays along with TCGA and public gene microarrays. The pooled SMD was 1.29 (95% CI: 1.09-1.48, I-square=78.6%, P<0.001) and the area under the curve (AUC) of the SROC was 0.88 (95%CI: 0.85-0.91). Compared to the upregulation of SYNJ2, SYNJ2 downregulation could improve OS in LUAD patients to some extent. SYNJ2 may facilitate the proliferation and progression of LUAD by modulating the cell cycle and TGF-beta signaling pathways. The 10 SYNJ2 co-expressed key genes selected from PPI network were all prominently implicated with the prognosis of LUAD patients. Conclusion SYNJ2 may contribute as an attractive and prospective therapeutic target in LUAD.

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“…For IHC staining of the xenografts, tumour tissues were fixed, embedded and sectioned (4 μm thick). Immunohistochemistry (IHC) staining for TMA and xenograft tissues was performed in accordance with previous procedures . The following antibodies were used as follows: primary antibody against SEZ6L2 (1:100) or cytochrome C (1:100) (Cell Signaling Technology) was used.…”

Section: Methodsmentioning

confidence: 99%

SEZ6L2 knockdown impairs tumour growth by promoting caspase‐dependent apoptosis in colorectal cancer

Zhao

Lan

et al. 2020

J Cellular Molecular Medi

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| 4223 wileyonlinelibrary.com/journal/jcmm | INTRODUC TI ONColorectal cancer (CRC) has been a common malignancy and leading cause of cancer mortality in the developed and developing countries, in recent years. 1 Epidemiological data in recent years suggest that the 5-year prevalence of CRC has reached 74.6 and 58.3 per 100 000 men and women, respectively. 2 According to the data, approximately 41% of all CRCs occur in the proximal colon, while 22% occur in the distal colon and 28% in the rectum. 2 With the advancements in understanding the pathogenesis, CRC is typically seen as a series of mutations and epigenetic changes that accumulate slowly, which may lead to a loss of function in tumour-suppressor genes and an increase in oncogenes. [3][4][5] Thus, understanding the function and mechanism of hub genes during CRC development AbstractSeizure-related 6 homolog (mouse)-like 2 (SEZ6L2) was shown to be involved in transcription of a type 1 transmembrane protein for regulating cell fate. Until now, the expression and function of SEZ6L2 in various cancers, including colorectal cancer (CRC), were unclear. In the present study, we determined the expression of SEZ6L2 in a tissue microarray from patients with CRC and then, analysed the correlation between SEZ6L2 expression and the prognosis of the patients. Furthermore, the potential function of SEZ6L2 in CRC was determined using cell counting kit, colony formation assay and xenograft model in vitro and in vivo. Flow cytometry, Western

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DDA1, a novel oncogene, promotes lung cancer progression through regulation of cell cycle

Cited by 15 publications

References 50 publications

TIPE1 function as a prognosis predictor and negative regulator of lung cancer

TIPE1 function as a prognosis predictor and negative regulator of lung cancer

The Clinical Significance and Potential Molecular Mechanisms of Synaptojanin 2 in Lung Adenocarcinoma

SEZ6L2 knockdown impairs tumour growth by promoting caspase‐dependent apoptosis in colorectal cancer

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