Peloruside A-Induced Cell Death in Hypoxia Is p53 Dependent in HCT116 Colorectal Cancer Cells

Řehulka, Jiří; Annadurai, Narendran; Frydrych, Ivo; Džubák, Petr; Miller, John H.; Hajdúch, Marián; Das, Viswanath

doi:10.1021/acs.jnatprod.7b00961

Cited by 5 publications

(3 citation statements)

References 27 publications

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“…Peloruside A was active against murine leukemia cells [236]. Peloruside A had no significant effect on its own on phosphorylation of tau but significantly increased the levels of acetyl tubulin in neuronal cell culture [237].…”

Section: Current Status Of Microtubule Stabilizersmentioning

confidence: 93%

Neuroprotective Approach of Anti-Cancer Microtubule Stabilizers Against Tauopathy Associated Dementia: Current Status of Clinical and Preclinical Findings

Duggal

Mehan

2019

ADR

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Neuronal microtubule (MT) tau protein provides cytoskeleton to neuronal cells and plays a vital role including maintenance of cell shape, intracellular transport, and cell division. Tau hyperphosphorylation mediates MT destabilization resulting in axonopathy and neurotransmitter deficit, and ultimately causing Alzheimer's disease (AD), a dementing disorder affecting vast geriatric populations worldwide, characterized by the existence of extracellular amyloid plaques and intracellular neurofibrillary tangles in a hyperphosphorylated state. Pre-clinically, streptozotocin stereotaxically mimics the behavioral and biochemical alterations similar to AD associated with tau pathology resulting in MT assembly defects, which proceed neuropathological cascades. Accessible interventions like cholinesterase inhibitors and NMDA antagonist clinically provides only symptomatic relief. Involvement of microtubule stabilizers (MTS) prevents tauopathy particularly by targeting MT oriented cytoskeleton and promotes polymerization of tubulin protein. Multiple in vitro and in vivo research studies have shown that MTS can hold substantial potential for the treatment of AD-related tauopathy dementias through restoration of tau function and axonal transport. Moreover, anti-cancer taxane derivatives and epothiolones may have potential to ameliorate MT destabilization and prevent the neuronal structural and functional alterations associated with tauopathies. Therefore, this current review strictly focuses on exploration of various clinical and pre-clinical features available for AD to understand the neuropathological mechanisms as well as introduce pharmacological interventions associated with MT stabilization. MTS from diverse natural sources continue to be of value in the treatment of cancer, suggesting that these agents have potential to be of interest in the treatment of AD-related tauopathy dementia in the future.

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Section: Current Status Of Microtubule Stabilizersmentioning

confidence: 93%

Neuroprotective Approach of Anti-Cancer Microtubule Stabilizers Against Tauopathy Associated Dementia: Current Status of Clinical and Preclinical Findings

Duggal

Mehan

2019

ADR

View full text Add to dashboard Cite

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“…Under hypoxic conditions, loss of the tumor suppressor p53 (encoded by TP53) provides cancer cells with a selective advantage, hypoxia which causes resistance to therapy and promotes metastasis in CRC. 205 , 206 Recently, Li et al reported the hypoxia inducible factor 1 alpha subunit (HIF1A) directly repressed the miRNA-34a in p53-defective CRC cells under hypoxia. 207 Conversely, p53 increases expression of miRNA-34a in CRC cells without hypoxia.…”

Section: Mechanisms/pathophysiologymentioning

confidence: 99%

Colorectal liver metastasis: molecular mechanism and interventional therapy

Zhou

Liu

Wang

et al. 2022

Sig Transduct Target Ther

128

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Colorectal cancer (CRC) is one of the most frequently occurring malignancy tumors with a high morbidity additionally, CRC patients may develop liver metastasis, which is the major cause of death. Despite significant advances in diagnostic and therapeutic techniques, the survival rate of colorectal liver metastasis (CRLM) patients remains very low. CRLM, as a complex cascade reaction process involving multiple factors and procedures, has complex and diverse molecular mechanisms. In this review, we summarize the mechanisms/pathophysiology, diagnosis, treatment of CRLM. We also focus on an overview of the recent advances in understanding the molecular basis of CRLM with a special emphasis on tumor microenvironment and promise of newer targeted therapies for CRLM, further improving the prognosis of CRLM patients.

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“…It is well known that cells are continuously disturbed by a vast variety of exogenous and endogenous stress, including oncogenes activation, unfolded proteins, genotoxic damage, physical impact, telomere erosion, and hypoxia, which disrupts the normal homeostasis of affected cells. (El-Khatib, Geara, Haddadin, & Gali-Muhtasib, 2010;Ou & Schumacher, 2018;Řehulka et al, 2018). As a key guardian of the genome, the tumor suppressor p53 is crucial for the cellular response DNA damaging stimuli to keep the genomic integrity of cells.…”

Section: Concluding Remarks and Future Perspectivesmentioning

confidence: 99%

Interferon‐stimulated gene 15 enters posttranslational modifications of p53

Wang

Ding

et al. 2018

Journal Cellular Physiology

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The tumor suppressor protein p53 is a central governor of various cellular signals. It is well accepted that ubiquitination as well as ubiquitin-like (UBL) modifications of p53 protein is critical in the control of its activity. Interferon-stimulated gene 15 (ISG15) is a well-known UBL protein with pleiotropic functions, serving both as a free intracellular molecule and as a modifier by conjugating to target proteins. Initially, attentions have historically focused on the antiviral effects of ISG15 pathway. Remarkably, a significant role in the processes of autophagy, DNA repair, and protein translation provided considerable insight into the new functions of ISG15 pathway. Despite the deterministic revelation of the relation between ISG15 and p53, the functional consequence of p53 ISGylation appears somewhat confused. More important, more recent studies have hinted p53 ubiquitination or other UBL modifications that might interconnect with its ISGylation. Here, we aim to summarize the current knowledge of p53 ISGylation and the differences in other significant modifications, which would be beneficial for the development of p53-based cancer therapy. K E Y W O R D S estrogen-responsive finger protein, HECT and RLD domain containing E3 ubiquitin protein ligase 5, p53 ISGylation, ubiquitin-like proteins

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Peloruside A-Induced Cell Death in Hypoxia Is p53 Dependent in HCT116 Colorectal Cancer Cells

Cited by 5 publications

References 27 publications

Neuroprotective Approach of Anti-Cancer Microtubule Stabilizers Against Tauopathy Associated Dementia: Current Status of Clinical and Preclinical Findings

Neuroprotective Approach of Anti-Cancer Microtubule Stabilizers Against Tauopathy Associated Dementia: Current Status of Clinical and Preclinical Findings

Colorectal liver metastasis: molecular mechanism and interventional therapy

Interferon‐stimulated gene 15 enters posttranslational modifications of p53

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