Endolysosomal Ca2+ Signalling and Cancer Hallmarks: Two-Pore Channels on the Move, TRPML1 Lags Behind!

Faris, Pawan; Shekha, Mudhir Sabir; Montagna, Daniela; Guerra, Germano; Moccia, Francesco

doi:10.3390/cancers11010027

Cited by 44 publications

(64 citation statements)

References 230 publications

(499 reference statements)

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“…TPCs are gated by multiple agonists, including nicotinic acid adenine dinucleotide phosphate (NAADP), sphingosine, and the EL phospholipid, phosphatidylinositol 3,5-bisphosphate (Galione 2019). TPCs-mediated Ca 2+ release recruits EL-located Ca 2+sensitive decoders, including calmodulin, synaptotagmin VII, and Arf6 (Faris et al 2018), to regulate vesicular fusion and trafficking (Galione 2019). A screening campaign aiming at repurposing FDA-approved drugs as novel antiviral compounds recently revealed that classical Ca 2+ antagonists blocked Ebola virus and MERS-CoV infections in vitro (Sakurai et al 2015;Gunaratne et al 2018a, b).…”

Section: Repurposing Of Clinically Available Antivirals To Treat Covimentioning

confidence: 99%

COVID-19-associated cardiovascular morbidity in older adults: a position paper from the Italian Society of Cardiovascular Researches

et al. 2020

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infects host cells following binding with the cell surface ACE2 receptors, thereby leading to coronavirus disease 2019 (COVID-19). SARS-CoV-2 causes viral pneumonia with additional extrapulmonary manifestations and major complications, including acute myocardial injury, arrhythmia, and shock mainly in elderly patients. Furthermore, patients with existing cardiovascular comorbidities, such as hypertension and coronary heart disease, have a worse clinical outcome following contraction of the viral illness. A striking feature of COVID-19 pandemics is the high incidence of fatalities in advanced aged patients: this might be due to the prevalence of frailty and cardiovascular disease increase with age due to endothelial dysfunction and loss of endogenous cardioprotective mechanisms. Although experimental evidence on this topic is still at its infancy, the aim of this position paper is to hypothesize and discuss more suggestive cellular and molecular mechanisms whereby SARS-CoV-2 may lead to detrimental consequences to the cardiovascular system. We will focus on aging, cytokine storm, NLRP3/inflammasome, hypoxemia, and air pollution, which is an emerging cardiovascular risk factor associated with rapid urbanization and globalization. We will finally discuss the impact of clinically available CV drugs on the clinical course of COVID-19 patients. Understanding the role played by SARS-CoV2

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Section: Repurposing Of Clinically Available Antivirals To Treat Covimentioning

confidence: 99%

COVID-19-associated cardiovascular morbidity in older adults: a position paper from the Italian Society of Cardiovascular Researches

et al. 2020

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“…With the identification of the molecular processes involved in pulmonary carcinogenesis, novel treatments targeting small molecules have emerged with encouraging results. For example, Ca 2+ signaling controls a wide variety of cell functions, such as secretion, gene transcription, cell proliferation and apoptosis [4][5][6]. Alterations of Ca 2+ signaling have emerged to an important factor in cancer progression [7,8].…”

Section: Introductionmentioning

confidence: 99%

Knockdown of STIM1 expression inhibits non-small-cell lung cancer cell proliferation in vitro and in nude mouse xenografts

Zeng

et al. 2019

Bioengineered

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Stromal interaction molecule 1 (STIM1) is a calcium-sensing protein localized in the membrane of the endoplasmic reticulum. The expression of STIM1 has been shown to be closely associated with cell proliferation. The aim of the present study was to investigate the role of STIM1 in the regulation of cancer progression and its clinical relevance. The data demonstrated that the expression of the STIM1 was significantly higher in non-small-cell lung cancer (NSCLC) tissues than in benign lesions and was associated with advanced NSCLC T stage. Knockdown of STIM1 expression in NSCLC cell lines A549 and SK-MES-1 significantly inhibited cell proliferation and induces A549 and SK-MES-1 cell arrest at the G2/M and S phases of the cell cycle. Western blotting showed that the expression of cyclin-dependent kinase (CDK) 1 and CDK2 were reduced while knockdown of STIM1 expression. Furthermore, knockdown of STIM1 in NSCLC cells significantly reduced the levels of xenograft tumor growth in nude mice. These data indicate that aberrant expression of the STIM1 protein may contribute to NSCLC progression. Future studies should focus on targeting STIM1 as a novel strategy for NSCLC therapy.

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“…Apart from the association of Wnt/β-catenin signaling with the induction of hepatoblastoma, studies have shown that the activation of this signaling also regulates hallmarks of tumor progression including degree of differentiation, invasiveness, metastasis [79]. The down-regulation of disheveled-2, a critical component of Wnt/β-catenin signaling pathway, has been associated with a decrease in the invasiveness of hepatoblastoma [80].…”

Section: Discussionmentioning

confidence: 99%

Wnt/β-catenin signaling as a useful therapeutic target in hepatoblastoma

et al. 2019

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Hepatoblastoma is a malignant tumor in the liver of children that generally occurs at the age of 2–3 years. There have been ample evidence from the preclinical as well as clinical studies suggesting the activation of Wnt/β-catenin signaling in hepatoblastoma, which is mainly attributed to the somatic mutations in the exon 3 of β-catenin gene. There is increased translocation of β-catenin protein from the cell surface to cytoplasm and nucleus and intracellular accumulation is directly linked to the severity of the cancer. Accordingly, the alterations in β-catenin and its target genes may be used as markers in the diagnosis and prognosis of pediatric live tumors. Furthermore, scientists have reported the therapeutic usefulness of inhibition of Wnt/β-catenin signaling in hepatoblastoma and this inhibition of signaling has been done using different methods including short interfering RNA (siRNA), miRNA and pharmacological agents. Wnt/β-catenin works in association with other signaling pathways to induce the development of hepatoblastoma including Yes-associated protein (YAP)1 (YAP-1), mammalian target of rapamycin (mTOR) 1 (mTOR-1), SLC38A1, glypican 3 (GPC3), nuclear factor κ-light-chain-enhancer of activated B cells (NF-kB), epidermal growth factor receptor, ERK1/2, tumor necrosis factor-α (TNF-α), regenerating islet-derived 1 and 3 α (REG1A and 3A), substance P (SP)/neurokinin-1 receptor and PARP-1. The present review describes the key role of Wnt/β-catenin signaling in the development of hepatoblastoma. Moreover, the role of other signaling pathways in hepatoblastoma in association with Wnt/β-catenin has also been described.

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Endolysosomal Ca2+ Signalling and Cancer Hallmarks: Two-Pore Channels on the Move, TRPML1 Lags Behind!

Cited by 44 publications

References 230 publications

COVID-19-associated cardiovascular morbidity in older adults: a position paper from the Italian Society of Cardiovascular Researches

COVID-19-associated cardiovascular morbidity in older adults: a position paper from the Italian Society of Cardiovascular Researches

Knockdown of STIM1 expression inhibits non-small-cell lung cancer cell proliferation in vitro and in nude mouse xenografts

Wnt/β-catenin signaling as a useful therapeutic target in hepatoblastoma

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