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Disorders of Keratinization and Other Genodermatoses
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Roselyn Stanger, Nanette Silverberg
Definition: The following two disorders are characterized by mutations in the phosphatase and tensin homolog (PTEN) tumor suppressor gene. PTEN negatively regulates the AKT/mTOR pathway, which is involved in cell growth and survival.
Markers of Sensitivity and Resistance to EGFR Inhibitors in Colorectal Cancer
Published in Sherry X. Yang, Janet E. Dancey, Handbook of Therapeutic Biomarkers in Cancer, 2021
Jose G. Monzon, Janet E. Dancey
PTEN (phosphatase and tensin homologue gene) encodes an enzyme that when functioning properly, signals cells to stop dividing and induces apoptosis when necessary. PTEN inactivation leads to uncontrolled signaling via PIP3 accumulation and subsequent AKT hyperphosphorylation, resulting in loss of responsiveness to apoptotic stimuli of cancer cells [128]. PTEN loss has been observed in different sporadic tumors, including colorectal cancers [129]. Preclinical data has demonstrated the importance of a functioning PTEN/PI3K/AKT pathway in determining the sensitivity of CRC cell lines to cetuximab [118].
Cowden Syndrome
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Among seven variants identified to date, CS1 accounts for 80% of clinical cases and shares with BRRS, PTEN-related Proteus syndrome, and Proteus-like syndrome in having PTEN mutations, which together are referred to as PTEN hamartoma tumor syndrome. The PTEN gene encodes a phosphatase that dephosphorylates the 3 position of phosphoinositide and thereby negatively controls the phosphoinositide 3-kinase–signaling pathway for regulating cell growth and survival. Mutations in the PTEN gene compromise its protein's function, leading to overproliferation of cells, hamartomatous growths, and predisposition to other cancers.
LncRNA IUR downregulates miR-144 to regulate PTEN in nasopharyngeal carcinoma
Published in Archives of Physiology and Biochemistry, 2023
Dan Liu, Hao Gong, Zezhang Tao, Shiming Chen, Yonggang Kong, Bokui Xiao
Phosphatase and tensin homolog (PTEN) is a phosphatase protein that plays a role as a tumour suppressor in cancer biology (Keniry and Parsons 2008). Mutations of PTEN are frequently observed during the development of many types of cancer (Alimonti et al.2010). In effect, some oncogenic miRNAs, such miR-144 can target PTEN to suppress cancer development, such as NPC (Zhang et al.2013). It has been well established that miRNAs can interact with other non-coding RNAs (ncRNAs), such as long (> 200 nt) ncRNAs (lncRNAs) to exert their roles (Jalali et al.2013). In NPC, certain differentially expressed lncRNAs have also been characterised as critical players in the development and progression of cancers (Liao et al.2019, Zhang et al.2019). IUR is a recently identified oncogenic lncRNA in leukaemia (Wang et al.2019). Our preliminary transcriptome analysis showed that IUR was downregulated in NPC and inversely correlated with miR-144, indicating the potential interactions between them in NPC. This study aimed to investigate the interactions among PTEN, miR-144 and IUR in NPC.
ELANE Promotes M2 Macrophage Polarization by Down-Regulating PTEN and Participates in the Lung Cancer Progression
Published in Immunological Investigations, 2023
Sinuo Song, Yunping Zhao, Tianyu Fu, Yunfei Fan, Jie Tang, Xiaoxing Wang, Chao Liu, Xiaobo Chen
In this study, we found that ELANE (concentration >40 nM) significantly down-regulated the expression of PTEN in M2 macrophages, and interference with PTEN expression could reverse the down-regulated expression of M2 macrophage markers induced by ELANE, suggesting that ELANE promoted the polarization of M2 macrophages by down-regulating PTEN expression. PTEN is a known tumor suppressor that is frequently inactivated in many human cancers, including lung cancer (Xiao et al. 2016). More and more studies have shown that the inactivation of PTEN contributes to the occurrence, development and malignant transformation of cancer. Emine et al. found that the down-regulation of PTEN expression in macrophages leads to the activation of CCAAT/enhancer binding protein β and signal transducer and activator of transcription (STAT) 3 signaling pathways, resulting in M2-type polarization (Sahin et al. 2014). However, the molecular mechanism of how PTEN regulates the polarization of M2 macrophages and influences the lung cancer progression needs to be elucidated urgently in the future.
The tumor microenvironment and triple-negative breast cancer aggressiveness: shedding light on mechanisms and targeting
Published in Expert Opinion on Therapeutic Targets, 2022
Natsuki Furukawa, Vered Stearns, Cesar A. Santa-Maria, Aleksander S. Popel
Several mechanisms have been proposed for the high expression level of PD-L1 in TNBC. In vitro study has shown that silencing of phosphatase and tensin homolog (PTEN) and the subsequent activation of the phosphoinositide 3-kinase (PI3K) signaling increase the expression level of PD-L1 in TNBC cells [30]. Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) is mutated in approximately 9% of TNBC tumors and is the second most frequently mutated gene. PTEN is also a highly mutated gene in TNBC [38]. CKLF-like MARVEL transmembrane domain containing protein 6 (CMTM6) was identified in a genome-wide CRISPR-Cas9 screen seeking genes required for PD-L1 expression. CMTM6 facilitates the recycling of PD-L1 to the cell surface and prevents degradation of PD-L1 in the lysosome [48]. Nucleophosmin (NPM1) is a transcriptional activator that binds to the PD-L1 promoter and increases its expression specifically in TNBC cell lines but not in non-invasive breast cancer cell lines [49].