P21-activated protein kinase 1 induces colorectal cancer metastasis involving ERK activation and phosphorylation of FAK at Ser-910

Li, Lianghui; Luo, Qi; Ye, Qing; Feng, Bo; Liu, Aiguo; Wang, Mingliang; Chen, Xuehua; Su, Liping; Liu, Bingya

doi:10.3892/ijo_00000746

Cited by 33 publications

(6 citation statements)

References 24 publications

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“…These cells reside in all tissues and organs and are capable of proliferating during the lifetime of the organism (Levi & Morrison 2008). Stem cells have been identified in the human thyroid gland (Thomas et al 2006, Lan et al 2007, Fierabracci et al 2008 and cancer stem cells in thyroid cancer cells and tissues (Mitsutake et al 2007, Todaro et al 2010, Zheng et al 2010, Malaguarnera et al 2011. Orthotopic transplantation of stem cells derived from undifferentiated thyroid cancer tissues into a mouse thyroid gland recapitulated the nature and behaviour of the original tumour, which supported the concept of stem cells being the source of tumour formation (Todaro et al 2010, Derwahl 2011.…”

Section: Introductionmentioning

confidence: 70%

Oestrogen action on thyroid progenitor cells: relevant for the pathogenesis of thyroid nodules?

Xu¹,

Chen²,

Peng³

et al. 2013

Journal of Endocrinology

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Benign and malignant thyroid nodules are more prevalent in females than in males. Experimental data suggest that the proliferative effect of oestrogen rather than polymorphisms is responsible for this gender difference. This study analysed whether both differentiated thyroid cells and thyroid stem and progenitor cells are targets of oestrogen action. In thyroid stem/progenitor cells derived from nodular goitres, the ability of 17b-oestradiol (E 2 ) to induce the formation of thyrospheres and the expression of oestrogen receptors (ERs) and the effect of E 2 on the growth and expression of markers of stem cells and thyroid differentiation (TSH receptor, thyroperoxidase, thyroglobulin and sodium iodide symporter (NIS)) were analysed. E 2 induced thyrosphere formation, albeit to a lower extent than other growth factors. Thyroid stem and progenitor cells expressed ERa (ESR1) and ERb (ESR2) with eight times higher expression levels of ERa mRNA compared with the differentiated thyrocytes. E 2 was a potent stimulator of the growth of thyroid stem/progenitor cells. In contrast, TSH-induced differentiation of progenitor cells, in particular, the expression of NIS, was significantly inhibited by E 2 . In conclusion, oestrogen stimulated the growth and simultaneously inhibited the differentiation of thyroid nodule-derived stem/progenitor cells. From these data and based on the concept of cellular heterogeneity, we hypothesize a supportive role of oestrogen in the propagation of thyroid stem/progenitor cells leading to the selection of a progeny of growth-prone cells with a decreased differentiation. These cells may be the origin of hypofunctioning or non-functioning thyroid nodules in females.

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Section: Introductionmentioning

confidence: 70%

Oestrogen action on thyroid progenitor cells: relevant for the pathogenesis of thyroid nodules?

Xu¹,

Chen²,

Peng³

et al. 2013

Journal of Endocrinology

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“…Stem cells are undifferentiated cells that possess the capacity of self-renewal and the generation of more differentiated progenitor cells (Davies et al 2011). These cells that reside in any organ and tissue for the lifetime of the organism have been detected in the human thyroid gland and in goiters and cancer stem cells in thyroid cancer cell lines and thyroid cancer tissues (Thomas et al 2006, Lan et al 2007, Mitsutake et al 2007, Fierabracci et al 2008, Todaro et al 2010, Zheng et al 2010, Malaguarnera et al 2011. Proliferation of stem cells is regulated by niches, signals from the surrounding microenvironment, which prevent the undifferentiated cells from undergoing uncontrolled cell division (Rezza et al 2014).…”

Section: Endocrine-related Cancermentioning

confidence: 99%

“…In differentiated thyroid cells and thyroid cancer cells, it has been demonstrated that apoptotic stimuli can overcome the control of niches, which in vitro in response to intense stimulation with growth factors results in the outgrowth of thyroid stem and progenitor cells as spheroids, designated thyrospheres, in vitro (Lan et al 2007, Fierabracci et al 2008, Zheng et al 2010.…”

Section: Endocrine-related Cancermentioning

confidence: 99%

Estrogen and its role in thyroid cancer

Derwahl¹,

Nicula²

2014

Endocrine Related Cancer

227

166

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Proliferative thyroid diseases are more prevalent in females than in males. Upon the onset of puberty, the incidence of thyroid cancer increases in females only and declines again after menopause. Estrogen is a potent growth factor both for benign and malignant thyroid cells that may explain the sex difference in the prevalence of thyroid nodules and thyroid cancer. It exerts its growth-promoting effect through a classical genomic and a non-genomic pathway, mediated via a membrane-bound estrogen receptor. This receptor is linked to the tyrosine kinase signaling pathways MAPK and PI3K. In papillary thyroid carcinomas, these pathways may be activated either by a chromosomal rearrangement of the tyrosine receptor kinase TRKA, by RET/PTC genes, or by a BRAF mutation and, in addition, in females they may be stimulated by high levels of estrogen. Furthermore, estrogen is involved in the regulation of angiogenesis and metastasis that are critical for the outcome of thyroid cancer. In contrast to other carcinomas, however, detailed knowledge on this regulation is still missing for thyroid cancer.

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“…Although PAKs are not mutated in cancerogenesis, they are overexpressed, hyperactivated, or amplified in several human tumors. PAK1 has been reported to be overexpressed in colorectal cancer, but its role in CRC remains unclear [82]. Some recent studies have implicated PAK's role in activation of Wnt-beta-catenin signaling through direct interaction and phosphorylation of betacatenin (see, e.g., [83]).…”

Section: Effects Of Vitamin D On Cell Proliferation Differentiationmentioning

confidence: 99%

Vitamin D and Colorectal Carcinogenesis

Juniku-Shkololli¹

2017

A Critical Evaluation of Vitamin D - Clinical Overview

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Colorectal cancer is the second leading cause of cancer-related death in the Western industrialized world. Many epidemiological studies have shown a negative association between colorectal cancer incidence and vitamin D levels. It has been suggested that the antitumoral action of 1,25(OH) 2 D 3 in colorectal cancer relies on several mechanisms at the cellular level. This prompted us to evaluate expression of certain immunohistochemical markers during tumor progression in colorectal human tissue and to study for the first time the relationship between histological type and grade of colorectal tumors with the expression of these markers. The investigated markers were the ones responsible for apoptosis (PAK1 and p53), cell adhesion (beta-catenin), differentiation (p53), and proliferation (Ki67). We also analyzed the correlation of their expression with vitamin D blood levels in these patients. Our results showed that the expression of these biomarkers increased with progression from colorectal adenomas to carcinomas. Expression of PAK1, beta-catenin, and p53 in the nucleus correlated with advanced stages of carcinoma. Low vitamin D blood levels correlated with nuclear accumulation of p53, nuclear beta-catenin expression, and expression of Ki67.

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P21-activated protein kinase 1 induces colorectal cancer metastasis involving ERK activation and phosphorylation of FAK at Ser-910

Cited by 33 publications

References 24 publications

Oestrogen action on thyroid progenitor cells: relevant for the pathogenesis of thyroid nodules?

Oestrogen action on thyroid progenitor cells: relevant for the pathogenesis of thyroid nodules?

Estrogen and its role in thyroid cancer

Vitamin D and Colorectal Carcinogenesis

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