NPTX1 inhibits colon cancer cell proliferation through down‐regulating cyclin A2 and CDK2 expression

Peng, Xing; Pan, Kangming; Zhao, Wei; Zhang, Jianzhu; Yuan, Shuiqiao; Wen, Xiang; Zhou, Wenquan; Zhou, Yu

doi:10.1002/cbin.10935

Cited by 40 publications

(31 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our data showed all the proliferation-related genes appeared to be up-regulated after the CYP19A1 knockdown. Previous studies have demonstrated that all of them play important regulatory roles in cell proliferation and the cell cycle ( 21 – 24 ). For example ( 25 ), found that neuron growth factors (NGF) promote the proliferation of granulosa cells (GC) by down-regulating ESR2 and CDKN1A.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of CYP19A1 in Buffalo Follicular Granulosa Cells Results in Increased Progesterone Secretion and Promotes Cell Proliferation

Duan

et al. 2020

Front. Vet. Sci.

View full text Add to dashboard Cite

Cytochrome P450 aromatase 19A1 (CYP19A1) is a critical enzyme in estrogen synthesis. However, the effect of CYP19A1 on cell growth and hormone secretion of buffalo follicular granulosa cells (BFGCs) is poorly understood. The objective of this study was to assess the role of CYP19A1 in cell proliferation and hormone secretion of BFGCs by knocking down CYP19A1 mRNA expression. The mRNA expression level of CYP19A1 gene was knocked down in BFGCs using the siCYP19A1-296 fragment with the best interference efficiency of 72.63%, as affirmed by real-time quantitative PCR (qPCR) and cell morphology analysis. The CYP19A1 knockdown promoted the proliferation of BFGCs through upregulating the mRNA expression levels of six proliferation-related genes (CCND1, CCNE1, CCNB1, CDK2, CDKN1A, and CDKN1B). Moreover, CYP19A1 knockdown increased (P < 0.05) the concentrations of progesterone secretion (P4) in BFGCs through increasing the mRNA expression levels of three steroidogenic genes (HSD17B1, HSD17B7, and CYP17A1). Our data further found that the FSH could inhibit the mRNA expression level of CYP19A1 in BFGCs, while LH obtains the opposite effect. These findings showed that the CYP19A1 knockdown had a regulatory role in the hormone secretion and cell proliferation in BFGCs.

show abstract

Section: Discussionmentioning

confidence: 99%

Knockdown of CYP19A1 in Buffalo Follicular Granulosa Cells Results in Increased Progesterone Secretion and Promotes Cell Proliferation

Duan

et al. 2020

Front. Vet. Sci.

View full text Add to dashboard Cite

show abstract

“…EdU incorporation assay was performed according to the method previously described ( 16 ). The EDU reagent was diluted to 5 μm in serum-free medium and added to the cells for 2 h. After PBS cleaning, 4% paraformaldehyde was added for 30 min and then 0.5% Triton X-100 was added for 20 min.…”

Section: Methodsmentioning

confidence: 99%

Downregulation of DUSP9 Promotes Tumor Progression and Contributes to Poor Prognosis in Human Colorectal Cancer

Qiu

Liang

Huang³

et al. 2020

Front. Oncol.

View full text Add to dashboard Cite

Background: Dual-specificity phosphatase 9 (DUSP9) belongs to the dual-specificity protein phosphatase subfamily. Recently, increasing attention has been paid on the role of DUSP9 in a variety of cancers. However, its functional role in tumor development is still unclear, especially in colorectal cancer (CRC). Methods: The functional role of DUSP9 in inhibiting the progression of CRC was verified using colony formation assay, wound healing assay, nude mice xenograft model, etc. RNA-seq was performed to assess the gene expression profiling in SW480 cells with DUSP9 stable knockdown and shControl cells. Bisulfite sequencing (BSE) was performed to reveal the methylation status of CpG island in the promoter of DUSP9. Results: DUSP9 was significantly downregulated in tumor tissues compared with peritumor tissues. Mechanistically, the high methylation status of CpG island in the promoter of DUSP9 may lead to the downregulation of DUSP9 in CRC. Clinically, low DUSP9 expression in CRC was closely associated with depth of invasion, metastasis (TNM) stage, and poor survival, indicating that DUSP9 may be involved in the progression of CRC. Functional study revealed that DUSP9 inhibited proliferation, migration, invasion, and epithelial-mesenchymal transition of CRC cells both in vitro and in vivo. Transcriptome profiling studies revealed that Erk signaling was involved in the tumor progression mediated by DUSP9 silencing, which is confirmed by cell experiments and clinical tissue sample staining analysis. Conclusion: Our findings demonstrate that DUSP9 plays a critical role in the progression of CRC, and therapeutic intervention to increase the expression or activity of DUSP9 may be a potential target for CRC treatment in the future.

show abstract

“…Upregulation of CDK2, the CDC25A phosphatase and DUSP14 in diabetes-free tumors is consistent with the tumor phenotype as these genes are reportedly overexpressed to stimulate cell proliferation and invasion in CRC [32][33][34]. Suppression of CSF1R expression both in diabetes-free and especially in diabetes tumors seems to be counter-productive for the malignancy via decreasing the influx of immunosuppressive tumor-associated macrophages (TAM) which in turn compromise antitumor activities of CD8+ cytotoxic lymphocytes [35].…”

Section: Discussionmentioning

confidence: 62%

Correlation between Expression Profiles of Key Signaling Genes in Colorectal Cancer Samples from Type 2 Diabetic and Non-Diabetic Patients

Elek

Rónai

Keszler

et al. 2020

Life

View full text Add to dashboard Cite

Several lines of epidemiological and biochemical evidence support the association of type 2 diabetes mellitus (T2DM) and colorectal cancer (CRC). T2DM has been shown to impinge on the transcriptome of colon tumor cells, promoting their proliferation and invasion. In order to gain insight into diabetes-specific modulation of colon cancer signaling, we analyzed gene expression patterns of more than five hundred genes encoding signaling proteins on TaqMan OpenArray panels from colonoscopic colorectal tumor samples of type 2 diabetic and non-diabetic patients. In total, 48 transcripts were found to be differentially expressed in tumors of T2DM patients as compared to healthy colon samples. Enrichment analysis with the g:GOSt (Gene Ontology Statistics) functional profiling tool revealed that the underlying genes can be classified into five signaling pathways (in decreasing order of significance: Wnt (wingless-type)/β-catenin; Hippo; TNF (tumor necrosis factor); PI3K/Akt (phosphoinositide-3 kinase/protein kinase B), and platelet activation), implying that targeted downregulation of these signaling cascades might help combat CRC in diabetic patients. Transcript levels of some of the differentially expressed genes were also measured from surgically removed diabetic and non-diabetic CRC specimens by individual qPCR (quantitative real-time PCR) assays using the adjacent normal tissue mRNA levels as an internal control. The most significantly altered genes in diabetic tumor samples were largely different from those in non-diabetic ones, implying that T2DM profoundly alters the expression of signaling genes and presumably the biological characteristics of CRC.

show abstract

NPTX1 inhibits colon cancer cell proliferation through down‐regulating cyclin A2 and CDK2 expression

Cited by 40 publications

References 30 publications

Knockdown of CYP19A1 in Buffalo Follicular Granulosa Cells Results in Increased Progesterone Secretion and Promotes Cell Proliferation

Knockdown of CYP19A1 in Buffalo Follicular Granulosa Cells Results in Increased Progesterone Secretion and Promotes Cell Proliferation

Downregulation of DUSP9 Promotes Tumor Progression and Contributes to Poor Prognosis in Human Colorectal Cancer

Correlation between Expression Profiles of Key Signaling Genes in Colorectal Cancer Samples from Type 2 Diabetic and Non-Diabetic Patients

Contact Info

Product

Resources

About