Mechanical Control of Epithelial-to-Mesenchymal Transitions in Development and Cancer

Przybyla, Laralynne; Muncie, Jonathon M.; Weaver, Valerie M.

doi:10.1146/annurev-cellbio-111315-125150

Cited by 117 publications

(75 citation statements)

References 183 publications

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“…EMT is a critical process in the development of numerous types of tissue and organs (27). The importance of EMT in mediating aggressiveness during carcinoma progression has attracted much attention in recent years (28).…”

Section: Discussionmentioning

confidence: 99%

ANXA1 affects cell proliferation, invasion and epithelial‑mesenchymal transition of oral squamous cell carcinoma

et al. 2017

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Abstract. Annexin A1 (ANXA1) acts either as a tumor suppressor or an oncogene in different tumor types. Several clinical studies revealed that the expression of ANXA1 is associated with the pathologic differentiation grade in oral squamous cell carcinoma (OSCC) patients. However, the direct function of ANXA1 in OSCC progression has remained to be fully clarified. The present study was designed to investigate the role of ANXA1 in OSCC cell proliferation and invasion in vitro. Furthermore, whether ANXA1 was involved in transforming growth factor β1 (TGFβ1)/epidermal growth factor (EGF)-induced epithelial-mesenchymal transition (EMT) in OSCC was explored. Tca-8113 and SCC-9 cells were transfected with ANXA1-pcDNA3.1 plasmid to overexpress ANXA1. Subsequently, cell proliferation and invasion were examined using MTT and Transwell-Matrigel invasion assays. TGFβ1 and EGF were used to induce EMT in Tca-8113 and SCC-9 cells, and the expression of epithelial (E)-cadherin, neural (N)-cadherin and vimentin was determined by western blot analysis. The results demonstrated that ANXA1 overexpression induced a significant decrease of cell growth and invasiveness in Tca-8113 and SCC-9 cells. The expression of E-cadherin was significantly increased, while the expression of vimentin and N-cadherin was significantly decreased in ANXA1-overexpressing Tca-8113 and SCC-9 cells. ANXA1 expression was significantly decreased in TGFβ1/EGF-treated cells. Furthermore TGFβ1/EGF-induced EMT in OSCC cell lines was attenuated by ANXA1 overexpression. In conclusion, to the best of our knowledge, the present study was the first to evidence that ANXA1 inhibits OSCC cell proliferation and invasion in vitro. TGFβ1/EGF-induced EMT was reversed by ANXA1 in OSCC. ANXA1 was suggested to be a potential marker for OSCC as well as a novel treatment.

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Section: Discussionmentioning

confidence: 99%

ANXA1 affects cell proliferation, invasion and epithelial‑mesenchymal transition of oral squamous cell carcinoma

et al. 2017

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“…This U-shaped tissue layer is eventually pinched off into a hollow neural tube, the early central nervous system (CNS), leaving behind neural crest cells outside of this tube that migrate to become the peripheral nervous system (PNS). Many of the cell rearrangements and migrations required for these processes are preceded by an epithelial-mesenchymal transition (EMT), which involves a shift from a collective static epithelial phenotype to an individual migratory phenotype (Przybyla et al, 2016b). Once cells arrive at the appropriate embryonic location, the reverse phenomenon, a mesenchymal-epithelial transition (MET), occurs (Nieto, 2013) as cells re-form an epithelial layer.…”

Section: Mechanical Forces Guide Brain Developmentmentioning

confidence: 99%

Tissue mechanics regulate brain development, homeostasis and disease

Barnes

Przybyla

Weaver

2017

Journal of Cell Science

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250

243

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All cells sense and integrate mechanical and biochemical cues from their environment to orchestrate organismal development and maintain tissue homeostasis. Mechanotransduction is the evolutionarily conserved process whereby mechanical force is translated into biochemical signals that can influence cell differentiation, survival, proliferation and migration to change tissue behavior. Not surprisingly, disease develops if these mechanical cues are abnormal or are misinterpreted by the cells – for example, when interstitial pressure or compression force aberrantly increases, or the extracellular matrix (ECM) abnormally stiffens. Disease might also develop if the ability of cells to regulate their contractility becomes corrupted. Consistently, disease states, such as cardiovascular disease, fibrosis and cancer, are characterized by dramatic changes in cell and tissue mechanics, and dysregulation of forces at the cell and tissue level can activate mechanosignaling to compromise tissue integrity and function, and promote disease progression. In this Commentary, we discuss the impact of cell and tissue mechanics on tissue homeostasis and disease, focusing on their role in brain development, homeostasis and neural degeneration, as well as in brain cancer.

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“…In non-small cell lung cancer, BANCR promotes the migration and invasion of cancer cells (8) through the mitogen-activated protein kinase (MAPK) signaling pathway. Epithelial-mesenchymal transition (EMT) refers to the process of transformation of epithelial cells to a mesenchymal cell phenotype, and serves an important function in tumor invasion and metastasis, since it may promote cancer cell migration and invasion (9,10). The association between BANCR and cellular migration, invasion, EMT and MAPK signaling in PTC remains unclear.…”

Section: Introductionmentioning

confidence: 99%

lncRNA BANCR promotes EMT in PTC via the Raf/MEK/ERK signaling pathway

Wang

Lin

et al. 2018

Oncol Lett

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Abstract. Thyroid cancer is one of the most common types of cancer in the endocrine system. Among all types of thyroid cancer, papillary thyroid carcinoma (PTC) is the most common type of thyroid cancer. Long non-coding RNA (lncRNA) BRAF-activated non-protein-coding RNA (BANCR) is a 688-bp-long nucleotide transcript, which was first identified in melanoma. The function of BANCR in thyroid cancer remains unclear. The aim of the present study was to investigate whether BANCR is involved in the development of thyroid cancer. The results indicated that BANCR expression was increased in thyroid tumors compared with in adjacent normal tissues. Among cancer cell lines, the expression level of BANCR differed: BANCR expression in BCPAP cell lines was lower compared with that in CAL-62, WRO and FTC-133 cell lines. Overexpression of BANCR promoted the migration and invasion of BCPAP cells. Additionally, BANCR mediated epithelial-mesenchymal transition (EMT) by regulating the expression of epithelial (E)-cadherin, vimentin and neuronal (N)-cadherin. Overexpression of BANCR in BCPAP cells decreased the expression of E-cadherin and increased the expression of vimentin, N-cadherin, phospho (p)-c-Raf, p-extracellular-signal-regulated kinase (ERK)/mitogen activated protein kinase (MEK)1/2 and p-ERK1/2. Administration of U0126 inhibitor inhibited the regulation of phosphorylation levels by MEK1/2 and ERK1/2. Additionally, U0126 upregulated the expression of E-cadherin and downregulated the expression of vimentin. Taken together, the results of the present study suggest that BANCR induces EMT in PTC through the Raf/MEK/ERK signaling pathway.

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Mechanical Control of Epithelial-to-Mesenchymal Transitions in Development and Cancer

Cited by 117 publications

References 183 publications

ANXA1 affects cell proliferation, invasion and epithelial‑mesenchymal transition of oral squamous cell carcinoma

ANXA1 affects cell proliferation, invasion and epithelial‑mesenchymal transition of oral squamous cell carcinoma

Tissue mechanics regulate brain development, homeostasis and disease

lncRNA BANCR promotes EMT in PTC via the Raf/MEK/ERK signaling pathway

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