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Knockdown of NCAPD3 inhibits the tumorigenesis of non-small cell lung cancer by regulation of the PI3K/Akt pathway

ABSTRACT: Knockdown of NCAPD3 inhibits the tumorigenesis of non-small cell lung cancer by regulation of the PI3K/Akt pathway

PROVIDER: PRJNA1049503 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27126025_1.fastq.gz	Fastqsanger.gz
	SRR27126025_2.fastq.gz	Fastqsanger.gz
	SRR27126026_1.fastq.gz	Fastqsanger.gz
	SRR27126026_2.fastq.gz	Fastqsanger.gz
	SRR27126027_1.fastq.gz	Fastqsanger.gz

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Knockdown of NCAPD3 inhibits the tumorigenesis of non-small cell lung cancer by regulation of the PI3K/Akt pathway

Project description:Background: Accumulating evidence indicates that aberrant non-SMC condensin II complex subunit D3 (NCAPD3) is associated with carcinogenesis of various cancers. Nevertheless, the biological role of NCAPD3 in the pathogenesis of non-small cell lung cancer (NSCLC) remains unclear.Methods: Immunohistochemistry and Western blot were performed to assess NCAPD3 expression in NSCLC tissues and cell lines. The ability of cell proliferation, invasion, and migration was evaluated by CCK-8 assays, EdU assays, Transwell assays, and scratch wound healing assays. Flow cytometry was performed to verify the cell cycle and apoptosis. RNA-sequence and rescue experiment were performed to reveal the underlying mechanisms.Results: The results showed that the expression of NCAPD3 was significantly elevated in NSCLC tissues. In NSCLC patients, high NCAPD3 expression was substantially associated with a worse prognosis. Functionally, knockdown of NCAPD3 resulted in cell apoptosis and cell cycle arrest in NSCLC cells as well as a significant inhibition of proliferation, invasion, and migration. Furthermore, RNA-sequencing analysis suggested that NCAPD3 contributes to NSCLC cancer carcinogenesis by regulating PI3K/Akt/FOXO4 pathway. Insulin-like growth factors-1 (IGF-1), a PI3K/Akt signaling activator, could reverse NCAPD3 silence-mediated proliferation inhibition and apoptosis in NSCLC cells.Conclusion: NCAPD3 suppresses apoptosis and promotes cell proliferation via the PI3K/Akt/FOXO4 signaling pathway, suggesting a potential use for NCAPD3 inhibitors as NSCLC therapeutics.

2024-02-14 | GSE249569 | GEO

EPDR1 inhibits proliferation and matastasis of ovarian cancer through PI3K/AKT pathway

Project description:Epithelial ovarian cancer (EOC) is the main subtype of ovarian cancer. In this study, we found that Ependymin-related 1 (EPDR1) was significantly downregulated in EOC tissues and low EPDR1 expression was associated with International Federation of Gynecology and Obstetrics (FIGO) stage, metastasis and poor prognosis. We confirmed that EPDR1 overexpression dramatically inhibited EOC cells proliferation, migration and invasion in vitro and in vivo. Mechanistically, EPDR1 suppressed EOC tumorigenesis and progression, at least in part, through inhibiting PI3K/AKT pathway. Furthermore, the expression and function were regulated by miR-429, as demonstrated by luciferase reporter assays and rescue experiments. In conclusion, our study demonstrated that EPDR1, negatively regulated by miR-429, played an important role in EOC development via PI3K/AKT pathway. The miR-429/EPDR1 axis might provide promising therapeutic targets for individualized treatment of EOC patients in future.

2021-11-18 | GSE188918 | GEO

Omipalisib Inhibits Esophageal Cancer Growth through PI3K/AKT/mTOR Signalling Pathway Disruption

Project description:Omipalisib Inhibits Esophageal Cancer Growth through PI3K/AKT/mTOR Signalling Pathway Disruption

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EPDR1 inhibits proliferation and matastasis of ovarian cancer through PI3K/AKT pathway

Project description:EPDR1 inhibits proliferation and matastasis of ovarian cancer through PI3K/AKT pathway

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KIF20A promotes the development of soft tissue sarcoma by activating the PI3K-AKT signaling pathway

Project description:Soft tissue sarcoma (STS) is a group of malignancies that can appear in any part of the body. The prognosis of STS patients remains unsatisfactory, mainly due to metastasis and recurrence. Upregulation of KIF20A is associated with poor prognosis of STS patients, but its downstream mechanism is unknown. In the present study, we found that downregulation of KIF20A in the STS cell line HT-1080 inhibits cell proliferation, migration, and invasion and induced cell apoptosis and G2/M arrest in vitro. In addition, downregulation of KIF20A in HT-1080 repressed tumorigenesis of STS in a xenograft mouse model. Pathway analysis showed, that downregulation of KIF20A led to suppression of downstream PI3K-AKT and NF-κB pathways. Specifically, the phosphorylation of AKT at Ser473 was inhibited. Taken together, our results indicate that KIF20A plays an important role in the development of STS by inhibiting cell proliferation, migration, invasion via the PI3K-AKT signaling pathway. Therefore, KIF20A is a potential therapeutic target in STS.

2020-11-23 | GSE140074 | GEO

Zearalenone exposure enhanced the expression of tumorigenesis genes in donkey granulosa cells via the PTEN/PI3K/AKT signaling pathway

Project description:We investigated the biological effects of ZEA exposure on donkey granulosa cells by using RNA-seq analysis. ZEA at 10 and 30 μM were administered to granulosa cells within 72 hours of in vitro culture. ZEA at 10 μM significantly altered the tumorigenesis associated genes in donkey granulosa cells. Exposure to 10 and 30 μM ZEA treatment significantly reduced mRNA expression of PTEN, TGFβ, ATM, and CDK2 genes, particularly, the ZEA treatment significantly increased the expression of PI3K and AKT genes. Furthermore, immunofluorescence, RT-qPCR, and Western blot analysis verified the gene expression of ZEA-exposed granulosa cells. Collectively, these results demonstrated the deleterious effect of ZEA exposure on the induction of ovarian cancer related genes via the PTEN/PI3K/AKT signaling pathway in donkey granulosa cells in vitro.

2018-07-12 | GSE116950 | GEO

Knockdown of HSPA13 inhibits TGFβ1-induced epithelial-mesenchymal transition of RPE by suppressing the PI3K/Akt signaling pathway

Project description:To investigate the effect of HSPA13 on TGFβ1-induced EMT of RPE cells, we performed bulk RNA sequencing (RNA-seq). Gene set enrichment analysis (GSEA) revealed that gene signatures associated with EMT and cell migration were significantly downregulated in the shHSPA13+TGFβ1 group relative to the shScramble+TGFβ1 group. PI3K/Akt signaling-related gene levels were repressed as well.

2024-09-04 | GSE264212 | GEO

Knockdown of CCNB2 inhibits the tumorigenesis of gastric cancer by regulation of the PI3K/Akt pathway.

Project description:Gastric cancer (GC) constitutes a malignant neoplasm with elevated mortality and dismal prognosis, featuring insidious early manifestation, a propensity for recurrence and metastasis, and drug resistance. Hence, there is an exigency to explore novel therapeutic tactics for GC. The expression of Cyclin B2 (CCNB2) is augmented in a multiplicity of human malignancies, nevertheless, investigations into the correlation between CCNB2 and GC are scarce. Our study reveal that CCNB2 is highly expressed in human GC tissues and significantly correlates with unfavorable survival prognoses in GC patients. Functional gain and loss assays demonstrated that CCNB2 can potentiate the proliferation and migration of GC cells both in vitro and in vivo, while its overexpression facilitates the epithelial-mesenchymal transition (EMT) process of GC cells. The outcomes of RNA sequencing imply that CCNB2 is implicated in the activation of the PI3K/AKT signaling pathway. Moreover, overexpression of RHBDL2 can countervail the inhibition of the EMT process and the PI3K/AKT signaling mediated by CCNB2 in GC cells. Thus, targeting this newly identified pathway might constitute a prospective therapeutic strategy for GC.

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TGFBR3 inhibits the aggressive of papillary thyroid cancer by inhibiting PI3K/AKT pathway and EMT

Project description:TGFBR3 inhibits the aggressive of papillary thyroid cancer by inhibiting PI3K/AKT pathway and EMT

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Valproic acid inhibits Burkitt lymphoma by downregulating PFN2 expression to modulate the PI3K/AKT pathway

Project description:Valproic acid inhibits Burkitt lymphoma by downregulating PFN2 expression to modulate the PI3K/AKT pathway

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