ADAM12 silencing promotes cellular apoptosis by activating autophagy in choriocarcinoma cells

Wang, Lin; Zhang, Ying; Keita, Nankoria Kady; Liu, Huining; Zhang, Yu

doi:10.3892/ijo.2020.5007

Cited by 6 publications

(7 citation statements)

References 82 publications

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“…Several genes have also been reported to play an oncogene role in choriocarcinoma cells. Wang et al have certified that ADAM1 depletion facilitates choriocarcinoma cell apoptosis via activating autophagy [ 15 ]. Zhao et al have found that aberrantly expressed SALL4 facilitates choriocarcinoma cell proliferation through the β -catenin/c-Myc pathway [ 16 ].…”

Section: Discussionmentioning

confidence: 99%

CBR3-AS1 Accelerates the Malignant Proliferation of Gestational Choriocarcinoma Cells by Stabilizing SETD4

Zhang

et al. 2022

Disease Markers

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Background. Gestational choriocarcinoma (GC) is a rare malignant gestational trophoblastic tumor. Long noncoding RNA (lncRNA) CBR3 antisense RNA 1 (CBR3-AS1) has been reported to serve as a critical oncogene and facilitate tumor progression. Besides, we found that CBR3-AS1 is implicated in GC progression. Materials and Methods. Gene and protein expression was detected via quantitative reverse transcription PCR (RT-qPCR) and western blot analyses, respectively. CCK-8 assay and colony formation assay were performed to assess cell proliferative abilities while flow cytometry analysis was applied for cell cycle and apoptosis. To analyze the specific mechanism among CBR3-AS1, SET domain containing 4 (SETD4), and polypyrimidine tract binding protein 1 (PTBP1), RNA binding protein immunoprecipitation (RIP), RNA pulldown, and mRNA stability assays were conducted. Results. CBR3-AS1 was markedly upregulated in GC cells, and its downregulation suppressed cell proliferation, induced cell cycle arrest, but promoted cell apoptosis in GC. SETD4 was determined as the downstream mRNA of CBR3-AS1 and positively regulated by CBR3-AS1 in GC cells. Furthermore, CBR3-AS1 could interact with its RNA binding protein (RBP) PTBP1, thereby stabilizing SETD4 mRNA. Rescue assays verified that CBR3-AS1 facilitates GC cell malignant proliferation via SETD4. Conclusion. CBR3-AS1 accelerates the malignant proliferation of GC cells via stabilizing SETD4.

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Section: Discussionmentioning

confidence: 99%

CBR3-AS1 Accelerates the Malignant Proliferation of Gestational Choriocarcinoma Cells by Stabilizing SETD4

Zhang

et al. 2022

Disease Markers

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“…Because it has been demonstrated that ADAM12 mediates cell proliferation through the activation of the PI3K/Akt/mTOR pathway, which is involved in several cellular functions and often contributes to oncogenesis [ 46 , 47 ], the phosphorylation levels of Akt ( Figure 6 A) and mTOR ( Figure 6 B) were investigated [ 48 ]. As shown in Figure 6 A, the treatment of 48 h with both concentrations of VNZ (100 nM or 1 µM) induced a significant increase in phospho-Akt (p-Akt) as compared to the VH group.…”

Section: Resultsmentioning

confidence: 99%

Effects of Subtoxic Concentrations of Atrazine, Cypermethrin, and Vinclozolin on microRNA-Mediated PI3K/Akt/mTOR Signaling in SH-SY5Y Cells

Graziosi

Sita

Corrieri

et al. 2022

IJMS

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Endocrine-disrupting chemicals (EDCs) are different natural and synthetic chemicals that may interfere with several mechanisms of the endocrine system producing adverse developmental, metabolic, reproductive, and neurological effects in both human beings and wildlife. Among pesticides, numerous chemicals have been identified as EDCs. MicroRNAs (miRNAs) can regulate gene expression, making fine adjustments in mRNA abundance and regulating proteostasis. We hypothesized that exposure to low doses of atrazine, cypermethrin, and vinclozolin may lead to effects on miRNA expression in SH-SY5Y cells. In particular, the exposure of SH-SY5Y cells to subtoxic concentrations of vinclozolin is able to downregulate miR-29b-3p expression leading to the increase in the related gene expression of ADAM12 and CDK6, which may promote a pro-oncogenic response through the activation of the PI3K/Akt/mTOR pathway and counteracting p53 activity. A better understanding of the molecular mechanisms of EDCs could provide important insight into their role in human disease.

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“…ADAM12 expression was previously reported to be high in breast, oesophageal, pituitary tumor, and choriocarcinoma [16,17,39] . Huang et al [16] found that lnc015192 competitively binds to miR-34a through sponging activity, inhibiting ADAM12 expression as well as tumour cell invasion, metastasis and the epithelial-to-mesenchymal transition.…”

Section: Discussionmentioning

confidence: 99%

ADAM12 as a Clinical Prognostic Indicator Associated with Tumour Immune Infiltration in Lung Adenocarcinoma

Pan

Huang

2021

Preprint

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Background: Lung cancer is the most common cause of cancer-related death worldwide. In humans, 22 functional α-disintegrinand metalloproteinases (ADAMs) have been identified, 12 of which have proteolytic activity. The role of ADAMs in cancer has attracted increasing attention. However, the expression and significance of ADAMs in lung adenocarcinoma (LUAD) remain unclear. The current study aimed to explore the expression and prognostic value of ADAM12 in LUAD.Methods: The Cancer Genome Atlas(TCGA) database was used to analyse the expression of ADAMs in LUAD. The cBioPortal database was used to obtain and analyse ADAM12 copy number changes, and the LinkedOmics database was utilised for the analysis of ADAM12-related genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis was then performed using TIMER. The relationship between ADAM12 and the tumour immune microenvironment(TIM) was assessed via the TISIDB database. ADAM12 and immune-related genes were used to construct a prognostic model. Knockdown of ADAM12 was performed in vitro in order to verify its biological function. The unpaired t-test was used for comparison between the two groups, ANOVA was used for analysing differences between multiple groups, and the Kaplan-Meier test was used to compare survival between groups.Results: Most ADAMs exhibited significant differential expression in LUAD. ADAM12 expression was significantly higher in LUAD tissues than in healthy tissues, and lower ADAM12 expression was associated with better survival. Genetic alterations of ADAM12 mainly included missense mutations, amplifications, and deep deletions. ADAM12 and positively correlated genes were mainly enriched in protein digestion and absorption, ECM-receptor interaction, and adhesion plaques. ADAM12 had a moderate correlation with immune cell markers EBIP1, CCNB1, EXO1, KNTC1, PRC1 and FAM198B. Prognostic model was established based on ADAM12 and immune-related genes. In vitro experiments revealed that knocking down ADAM12 inhibited cell proliferation, migration and invasion.Conclusion: ADAM12 potentially plays an important role in the occurrence of LUAD and may be utilised as an immunotherapy target and a valuable prognostic biomarker for LUAD.

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ADAM12 silencing promotes cellular apoptosis by activating autophagy in choriocarcinoma cells

Cited by 6 publications

References 82 publications

CBR3-AS1 Accelerates the Malignant Proliferation of Gestational Choriocarcinoma Cells by Stabilizing SETD4

CBR3-AS1 Accelerates the Malignant Proliferation of Gestational Choriocarcinoma Cells by Stabilizing SETD4

Effects of Subtoxic Concentrations of Atrazine, Cypermethrin, and Vinclozolin on microRNA-Mediated PI3K/Akt/mTOR Signaling in SH-SY5Y Cells

ADAM12 as a Clinical Prognostic Indicator Associated with Tumour Immune Infiltration in Lung Adenocarcinoma

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