Downregulation of Diacylglycerol kinase zeta (DGKZ) suppresses tumorigenesis and progression of cervical cancer by facilitating cell apoptosis and cell cycle arrest

Liu, Keying; Xue, Biyun; Bai, Guiqin; Zhang, Wentao

doi:10.1080/21655979.2021.1918505

Cited by 13 publications

(8 citation statements)

References 36 publications

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“…Similarly, SRSF2 knockdown partially rescued the AASE events in the DGKZ gene (Fig. 5h ), which is involved in carcinogenesis and immune response 55 , 56 , while knocking down three other upregulated SFs ( SRSF1 , SRSF3 , and HNRNPD ) had no effects (Supplementary Fig. S9d ).…”

Section: Resultsmentioning

confidence: 87%

Wiskott-Aldrich syndrome protein forms nuclear condensates and regulates alternative splicing

et al. 2022

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The diverse functions of WASP, the deficiency of which causes Wiskott-Aldrich syndrome (WAS), remain poorly defined. We generated three isogenic WAS models using patient induced pluripotent stem cells and genome editing. These models recapitulated WAS phenotypes and revealed that WASP deficiency causes an upregulation of numerous RNA splicing factors and widespread altered splicing. Loss of WASP binding to splicing factor gene promoters frequently leads to aberrant epigenetic activation. WASP interacts with dozens of nuclear speckle constituents and constrains SRSF2 mobility. Using an optogenetic system, we showed that WASP forms phase-separated condensates that encompasses SRSF2, nascent RNA and active Pol II. The role of WASP in gene body condensates is corroborated by ChIPseq and RIPseq. Together our data reveal that WASP is a nexus regulator of RNA splicing that controls the transcription of splicing factors epigenetically and the dynamics of the splicing machinery through liquid-liquid phase separation.

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Section: Resultsmentioning

confidence: 87%

Wiskott-Aldrich syndrome protein forms nuclear condensates and regulates alternative splicing

et al. 2022

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“…Then, we further probed whether fluvastatin exerted protective effects on EC progression via knocking down SIRT6 expression. However, the role of PI3K-mTOR pathway in the mechanism of action of fluvastatin related to SIRT6 still requires further study [ 23 , 24 ]. It was obviously found that depletion of SIRT6 triggered more activated cell viability and stimulated the behaviors of EC cells, including proliferation, migration, invasion.…”

Section: Discussionmentioning

confidence: 99%

Fluvastatin suppresses the proliferation, invasion, and migration and promotes the apoptosis of endometrial cancer cells by upregulating Sirtuin 6 (SIRT6)

Cai

Zhao

2021

Bioengineered

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Fluvastatin, the first fully synthesized 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (HMGCR) inhibitor, has been reported to inhibit the development and metastasis of multiple cancers. The present study aimed to explore the effects of fluvastatin on endometrial cancer (EC) as well as reveal its potential mechanism. After exposure to fluvastatin, the cell viability, proliferation, migration, and invasion of EC cells were measured by Cell Counting Kit-8 (CCK-8), 5-ethynyl-2ʹ-deoxyuridine (EDU), wound healing, and invasion assays, respectively. The apoptosis and its related proteins of fluvastatin-treated EC cells were detected by TUNEL and Western blot, separately. In order to figure out the effects of SIRT6 silence on EC cells, a series of cellular activities were performed again. Fluvastatin suppressed the proliferation, migration, and invasion of EC cells, but induced the apoptosis. The expression of SIRT6 was elevated in EC cells upon fluvastatin exposure. After silencing SIRT6 in fluvastatin-treated EC cells, the proliferation, migration, and invasion were promoted whereas the apoptosis was decreased. To sum up, this study firstly evidenced that fluvastatin suppresses the proliferation, invasion, and migration and promotes the apoptosis of endometrial cancer cells by regulating SIRT6 expression.

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“…At the cellular level, tumorigenesis is considered to involve disruption of the balance between cell proliferation and apoptosis 31,32 . Dysfunction of programmed cell death enables tumor cells to survive oxidative stress or hypoxia; thus, apoptosis is closely associated with tumor pathogenesis 33 . In this study, we examined the effect of high/low TIGD1 expression on the proliferation of two different OSCC cell lines.…”

Section: Discussionmentioning

confidence: 99%

A novel oncogene trigger transposable element derived‐1 promotes oral squamous cell carcinoma progression via evoking immune inhibition

Qin

Zhu

Song

et al. 2023

Molecular Carcinogenesis

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Oral squamous cell carcinoma (OSCC) is one of the most common head and neck squamous cell carcinomas (HNSCC) globally. Its incidence rate is rapidly increasing, and its 5‐year survival rate remains at 50%, despite advances in medical science. Trigger transposable element‐derived 1 (TIGD1) has been found to be upregulated in various cancer types. However, its biological function in OSCC requires further investigation. We searched the Cancer Genome Atlas database using CIBERSORT and TIMER 2.0 to predict the significance of TIGD1 and evaluate its effect on immune cell infiltration. Gene set enrichment analysis was performed to determine the biological functions of TIGD1. Gain/loss of function techniques were used to explore the biological behavior of TIGD1 in Cal27 and HSC4 cells. Finally, flow cytometry was used to detect dendritic cell markers in an OSCC and dendritic cell co‐culture model. Our results show that TIGD1 is upregulated significantly in OSCC and is closely associated with tumor progression and prognosis. TIGD1 functions as an oncogene by increasing cells proliferation, inhibiting apoptosis, promoting cell invasion and migration. TIGD1 is also involved in tumor immune cell infiltration. Its overexpression can inhibit dendritic cell maturation, leading to immune suppression and tumor progression. High TIGD1 expression, which promotes OSCC progression, might be related to decreased dendritic cell maturation and activation. These findings suggest that TIGD1‐specific small interfering RNA synthesized in vitro could be a new target for OSCC immunotherapy.

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Downregulation of Diacylglycerol kinase zeta (DGKZ) suppresses tumorigenesis and progression of cervical cancer by facilitating cell apoptosis and cell cycle arrest

Cited by 13 publications

References 36 publications

Wiskott-Aldrich syndrome protein forms nuclear condensates and regulates alternative splicing

Wiskott-Aldrich syndrome protein forms nuclear condensates and regulates alternative splicing

Fluvastatin suppresses the proliferation, invasion, and migration and promotes the apoptosis of endometrial cancer cells by upregulating Sirtuin 6 (SIRT6)

A novel oncogene trigger transposable element derived‐1 promotes oral squamous cell carcinoma progression via evoking immune inhibition

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