Knockdown of TMEM45B inhibits cell proliferation and invasion in gastric cancer

Shen, Kexin; Yu, Wei; Yu, Yanhui; Liu, Xiumin; Cui, Xiaofeng

doi:10.1016/j.biopha.2018.05.016

Cited by 31 publications

(20 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These effects were associated with a decrease in the expression of β-catenin, cyclin D1 and c-Myc (Li et al, 2017). Similar results were obtained in gastric cancer cells, in which TMEM45B silencing was associated with a decrease in the abundance of p-STAT3 and p-JAK2 (Shen et al, 2018). These two proteins can be described as potential prognosis markers but also as regulators of tumor growth in several types of cancer.…”

Section: Part 2: Tmems As Oncogenessupporting

confidence: 77%

TMEM Proteins in Cancer: A Review

2018

View full text Add to dashboard Cite

A transmembrane protein (TMEM) is a type of protein that spans biological membranes. Many of them extend through the lipid bilayer of the plasma membrane but others are located to the membrane of organelles. The TMEM family gathers proteins of mostly unknown functions. Many studies showed that TMEM expression can be down- or up-regulated in tumor tissues compared to adjacent healthy tissues. Indeed, some TMEMs such as TMEM48 or TMEM97 are defined as potential prognostic biomarkers for lung cancer. Furthermore, experimental evidence suggests that TMEM proteins can be described as tumor suppressors or oncogenes. TMEMs, such as TMEM45A and TMEM205, have also been implicated in tumor progression and invasion but also in chemoresistance. Thus, a better characterization of these proteins could help to better understand their implication in cancer and to allow the development of improved therapy strategies in the future. This review gives an overview of the implication of TMEM proteins in cancer.

show abstract

Section: Part 2: Tmems As Oncogenessupporting

confidence: 77%

TMEM Proteins in Cancer: A Review

2018

View full text Add to dashboard Cite

show abstract

“…TMEM45B is abnormally expressed in many types of tumors. Knockdown of TMEM45B can inhibit the JAK2/STAT3 signaling pathway, thereby inhibiting the proliferation, migration, and invasion of GC cells [47]. PXMP2 plays a vital role in lipid and reactive oxygen metabolism, which is [在此处键入] a new target for studying depression [48], but its effect in tumors has not been reported.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics analysis of aberrantly methylated- differentially expressed genes in gastric cancer

Siyuan

Shu

2021

Preprint

View full text Add to dashboard Cite

Background: This study was carried out to identify the aberrantly methylated-differentially expressed genes in gastric cancer (GC). Methods: We downloaded data of gene expression microarrays GSE118916 and gene methylation microarrays GSE25869 from the Gene Expression Omnibus (GEO) database. The DEGs and DMGs were analyzed by the limma software package and Venn diagram. The PPI network was mapped and the enrichment analysis was conducted by the DAVID database. GEPIA online tool, Oncomine database, HPA, and cBioPortal tool were used to verify hub genes. Result: We obtained 110 Hypo-HGs, 9 high-regulation hypomethylation oncogenes, 23 Hyper-LGs, and 2 low-regulation hypermethylation tumor suppressor genes. Hypo-HGs biological process mainly involves cell adhesion and extracellular matrix organization, Hyper-LGs biological process mainly involves response to nicotine and xenobiotic metabolic process. KEGG analysis showed that Hypo-HGs significantly enriched in Focal adhesion, PI3K-Akt signaling pathway, and ECM-receptor interaction. Hyper-LGs significantly enriched in Drug metabolism-cytochrome P450, Chemical carcinogenesis, and Metabolism of xenobiotics by cytochrome P450. The database identified the hub genes were COL1A1, THBS1, COL5A2, COL12A1, and CXCR. Conclusion: COL1A1, THBS1, COL5A2, COL12A1, and CXCR4 can be used as a target for precise diagnosis and treatment of GC. Focal adhesion, PI3K-Akt signaling pathway, and ECM-receptor interaction are important mechanisms of GC.

show abstract

“…In contrast, few TMEM are upregulated in cancer, and these function as oncogenes. For example, TMEM17 and TMEM45B are associated with poor prognosis in cancer. However, the TMEM family involves various proteins whose functions are mostly unknown, and P7TP3 is one of them.…”

Section: Discussionmentioning

confidence: 99%

P7TP3 inhibits tumor development, migration, invasion and adhesion of liver cancer through the Wnt/β‐catenin signaling pathway

et al. 2020

View full text Add to dashboard Cite

The effect of hepatitis C virus p7 trans‐regulated protein 3 (P7TP3) in the development of hepatocellular carcinoma (HCC) is still unknown. The present study aimed to investigate the role and mechanism of P7TP3 in HCC. P7TP3 was significantly decreased in HCC tissues when compared with corresponding liver tissues immediately around the tumor (LAT) from seven HCC patients. Fewer and smaller colonies originated from HepG2‐P7TP3 cells when compared to HepG2‐NC cells. Overexpression of P7TP3 in HepG2 cells significantly repressed the growth of HCC xenografts in nude mice. Furthermore, wound‐healing tests, Transwell assays, Matrigel Transwell assays, adhesion assays, CCK‐8 assays, flow cytometry and western blotting analysis showed that P7TP3 protein expression inhibited migration, invasion, adhesion, proliferation and cell cycle progression in HCC cell lines. Moreover, P7TP3 suppressed the activity of the Wnt/β‐catenin signaling pathway, and was restored by Wnt3a, which is an activator of the Wnt/β‐catenin signaling pathway. Consistently, β‐catenin was highly expressed by P7TP3 silencing, and restored by XAV939, an inhibitor of the Wnt/β‐catenin signaling pathway. Finally, microRNA (miR)‐182‐5p suppressed the expression of target gene P7TP3 by directly interacting with the 3′‐UTR region. Taken together, P7TP3, the direct target gene of miR‐182‐5p, inhibited HCC by regulating migration, invasion, adhesion, proliferation and cell cycle progression of liver cancer cell through the Wnt/β‐catenin signaling pathway. These findings provide strong evidence that P7TP3 functions as a new promising tumor suppressor in HCC.

show abstract

Knockdown of TMEM45B inhibits cell proliferation and invasion in gastric cancer

Cited by 31 publications

References 23 publications

TMEM Proteins in Cancer: A Review

TMEM Proteins in Cancer: A Review

Bioinformatics analysis of aberrantly methylated- differentially expressed genes in gastric cancer

P7TP3 inhibits tumor development, migration, invasion and adhesion of liver cancer through the Wnt/β‐catenin signaling pathway

Contact Info

Product

Resources

About