Expression of PTEN‑long nephritis and its effect on renal inflammation

Wang, Hui; Q, Yu; Wang, Lin; Li, Yongwei; Xie, Mao; Lu, Youyi; Cui, Yaya

doi:10.3892/etm.2018.7049

Cited by 3 publications

(2 citation statements)

References 32 publications

(31 reference statements)

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“… 65 Cao and colleagues 14 showed that cells expressing only PTEN-L synthesised the highest levels of C-X-C motif chemokine ligand (CXCL) 10 and the pro-inflammatory cytokines interleukin (IL)-6 and CXCL1. In addition, Wang and colleagues 66 demonstrated that the knockdown of PTEN - L significantly reduced the expression of TNFα and IL-6, which both have a pro-inflammatory role in mediating immune response. In this context, loss of PTEN and its secreted variant PTEN-L in tumour cells is likely to increase the activity of immunosuppressive cytokines on the immune cells in the TME.…”

Section: Pten and The Immune Responsementioning

confidence: 99%

Emerging role of PTEN loss in evasion of the immune response to tumours

et al. 2020

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Mutations in PTEN activate the phosphoinositide 3-kinase (PI3K) signalling network, leading to many of the characteristic phenotypic changes of cancer. However, the primary effects of this gene on oncogenesis through control of the PI3K–AKT–mammalian target of rapamycin (mTOR) pathway might not be the only avenue by which PTEN affects tumour progression. PTEN has been shown to regulate the antiviral interferon network and thus alter how cancer cells communicate with and are targeted by immune cells. An active, T cell-infiltrated microenvironment is critical for immunotherapy success, which is also influenced by mutations in DNA damage repair pathways and the overall mutational burden of the tumour. As PTEN has a role in the maintenance of genomic integrity, it is likely that a loss of PTEN affects the immune response at two different levels and might therefore be instrumental in mediating failed responses to immunotherapy. In this review, we summarise findings that demonstrate how the loss of PTEN function elicits specific changes in the immune response in several types of cancer. We also discuss ongoing clinical trials that illustrate the potential utility of PTEN as a predictive biomarker for immune checkpoint blockade therapies.

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Section: Pten and The Immune Responsementioning

confidence: 99%

Emerging role of PTEN loss in evasion of the immune response to tumours

et al. 2020

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“…In ccRCC cells, the tumor suppressor gene PTEN activates the PI3K cascade via p53-mediated transactivation, while NOTCH1 cascade regulation increases the level of PTEN and induces increased expression of participating lipid biosynthases, including ACLY, FASN and ACC. However, it has recently been found that accumulation of NADH leads to PTEN inactivation 23 , 24 .…”

Section: Metabolic Reprogramming In Tumor Cellsmentioning

confidence: 99%

Role of Metabolic Reprogramming of Long non-coding RNA in Clear Cell Renal Cell Carcinoma

Zhang¹,

Yu²,

Chen³

et al. 2022

J. Cancer

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Renal cell carcinoma (RCC), one of the most frequent cancers, is a "classical" malignancy characterized by metabolic reprogramming. Clear cell renal cell carcinoma (ccRCC) is its most common histopathological subtype. Long-stranded non-coding ribonucleic acids (LncRNAs) are regulatory RNA molecules with limited protein-coding capacity and evolutionary conservation. Recent studies have revealed that lncRNAs can broadly regulate the metabolic reprogramming of ccRCC and its malignant transformation. However, there are few studies on lncRNAs regulating the metabolism of ccRCC, and the specific mechanisms are unknown. Therefore, this paper summarizes the regulatory mechanisms of lncRNAs in the metabolism of ccRCC, especially in the pathways of glycolysis, mitochondrial function, glutamine and lipid metabolism, cellular mechanisms, interactions with other molecules, specific scientific and clinic implications and applications to provide a basis for early clinical diagnosis, prediction and treatment. We also discuss the clinical application and challenges of targeting lncRNAs in ccRCC metabolism.

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