Crosslink between p53 and metastasis: focus on epithelial–mesenchymal transition, cancer stem cell, angiogenesis, autophagy, and anoikis

Babaei, Ghader; Aliarab, Azadeh; Vostakolaei, Mehdi Asghari; Hotelchi, Masumeh; Neisari, Roghaiyeh; Bazl, Masumeh Rajabi

doi:10.1007/s11033-021-06706-1

Cited by 15 publications

(11 citation statements)

References 76 publications

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“…P53 (TP53), as a tumor suppressor, is thought to be the most frequently mutated gene in cancer cells. There is increasing evidence that mutated p53 enhances tumor metastasis and affects EMT processes [139]. Moreover, a large number of recent studies have shown that p53 signaling plays a role in regulating the EMT process in lung cancer [140][141][142][143].…”

Section: Other Signaling Pathwaysmentioning

confidence: 99%

The effects of epithelial–mesenchymal transitions in COPD induced by cigarette smoke: an update

Zhu

Lin

et al. 2022

Respir Res

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Cigarette smoke is a complex aerosol containing a large number of compounds with a variety of toxicity and carcinogenicity. Long-term exposure to cigarette smoke significantly increases the risk of a variety of diseases, including chronic obstructive pulmonary disease (COPD) and lung cancer. Epithelial–mesenchymal transition (EMT) is a unique biological process, that refers to epithelial cells losing their polarity and transforming into mobile mesenchymal cells, playing a crucial role in organ development, fibrosis, and cancer progression. Numerous recent studies have shown that EMT is an important pathophysiological process involved in airway fibrosis, airway remodeling, and malignant transformation of COPD. In this review, we summarized the effects of cigarette smoke on the development and progression of COPD and focus on the specific changes and underlying mechanisms of EMT in COPD induced by cigarette smoke. We spotlighted the signaling pathways involved in EMT induced by cigarette smoke and summarize the current research and treatment approaches for EMT in COPD, aiming to provide ideas for potential new treatment and research directions.

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Section: Other Signaling Pathwaysmentioning

confidence: 99%

The effects of epithelial–mesenchymal transitions in COPD induced by cigarette smoke: an update

Zhu

Lin

et al. 2022

Respir Res

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“…Dysregulations of the TME contributing to the angiogenic switch have been linked to distinct mechanisms including anomalous expression levels of HIF-1, pro-angiogenic factors VEGF and bFGF as well as anti-angiogenic factors such as thrombospondin-1 (TSP-1) ( 83 , 84 ). The tumour suppressor gene p53 regulates these factors and mediates cellular functions such as apoptosis, DNA repair, cell cycle development and angiogenesis inhibition ( 83 ).…”

Section: Regulating Genes Of the Tumour Vasculaturementioning

confidence: 99%

“…Therefore, p53 mutations may lead to both increased HIF-1α and HIF-1β expression, thereby promoting angiogenesis by upregulating factors such as VEGF ( 86 ). Furthermore, p53 mutations have also been demonstrated to upregulate VEGF expression in human colon, bladder, and breast cancer surgical specimens as p53 acts directly on the VEGF promoter region ( 44 , 84 ).…”

Section: Regulating Genes Of the Tumour Vasculaturementioning

confidence: 99%

“…Additionally, the anti-angiogenic ECM glycoprotein TSP-1 is implicated in reducing cancer cell proliferation, survival as well as motility and is upregulated by p53 binding to the encoding THBS1 promoter region ( 84 , 87 , 88 ). This suggests that p53 mutations downregulating TSP-1 may further contribute to the formation of abnormal tumour vasculature ( 84 , 88 ).…”

Section: Regulating Genes Of the Tumour Vasculaturementioning

confidence: 99%

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The mechanistic immunosuppressive role of the tumour vasculature and potential nanoparticle-mediated therapeutic strategies

et al. 2022

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The tumour vasculature is well-established to display irregular structure and hierarchy that is conducive to promoting tumour growth and metastasis while maintaining immunosuppression. As tumours grow, their metabolic rate increases while their distance from blood vessels furthers, generating a hypoxic and acidic tumour microenvironment. Consequently, cancer cells upregulate the expression of pro-angiogenic factors which propagate aberrant blood vessel formation. This generates atypical vascular features that reduce chemotherapy, radiotherapy, and immunotherapy efficacy. Therefore, the development of therapies aiming to restore the vasculature to a functional state remains a necessary research target. Many anti-angiogenic therapies aim to target this such as bevacizumab or sunitinib but have shown variable efficacy in solid tumours due to intrinsic or acquired resistance. Therefore, novel therapeutic strategies such as combination therapies and nanotechnology-mediated therapies may provide alternatives to overcoming the barriers generated by the tumour vasculature. This review summarises the mechanisms that induce abnormal tumour angiogenesis and how the vasculature’s features elicit immunosuppression. Furthermore, the review explores examples of treatment regiments that target the tumour vasculature.

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“…Imbalance of angiogenic and angiostatic markers that forms pathologic angiogenesis supplies the vital need of any growing malignant tissue. Compensatory mechanisms within non-small-cell lung carcinoma (NSCLC) overexpress endothelial growth factor (VEGF) and its receptor (VEGFR-2) that are the major responsible for pathologic angiogenic surge within the tumor [3] . EGF (Epidermal growth factor) which stabilizes hypoxia-inducible factor (HIF) leads to more angiogenesis transcription, cancer cell division and progression [4] .…”

Section: Introductionmentioning

confidence: 99%

Recovering the angiogenic/angiostatic balance in NNK-induced lung carcinoma via 12 weeks of submaximal swimming and Nigella sativa nanocapsule

et al. 2022

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Crosslink between p53 and metastasis: focus on epithelial–mesenchymal transition, cancer stem cell, angiogenesis, autophagy, and anoikis

Cited by 15 publications

References 76 publications

The effects of epithelial–mesenchymal transitions in COPD induced by cigarette smoke: an update

The effects of epithelial–mesenchymal transitions in COPD induced by cigarette smoke: an update

The mechanistic immunosuppressive role of the tumour vasculature and potential nanoparticle-mediated therapeutic strategies

Recovering the angiogenic/angiostatic balance in NNK-induced lung carcinoma via 12 weeks of submaximal swimming and Nigella sativa nanocapsule

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