Epithelial-mesenchymal transition in cancer: An overview

Ramos, Fabiano Santos; Wons, Letícia; Cavalli, Iglenir João; Ribeiro, Enilze M.S.F.

doi:10.15761/icst.1000243

Cited by 14 publications

(8 citation statements)

References 66 publications

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“…Epithelial-mesenchymal transition (EMT) is the process by which polarized epithelial cells of the basement membrane sustain various biochemical modifications to become phenotypically mesenchymal [ 24 , 25 , 26 ]. Mesenchymal cells are capable of cellular processes such as migration and invasion, and become more resistant to apoptosis, thus making it an important development in associated physiological processes.…”

Section: Epithelial Mesenchymal Transition (Emt)mentioning

confidence: 99%

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The Developmental Origins of Cancer: A Review of the Genes Expressed in Embryonic Cells with Implications for Tumorigenesis

Balachandran

Narendran

2023

Genes

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Tumorigenesis, which involves the uncontrolled proliferation and differentiation of cells, has been observed to imitate a variety of pathways vital to embryonic development, motivating cancer researchers to explore the genetic origins of these pathways. The pluripotency gene regulatory network is an established collection of genes that induces stemness in embryonic cells. Dysregulation in the expression genes of the pluripotency gene networks including OCT4, SOX2, NANOG and REX1 have been implicated in tumor development, and have been observed to result in poorer patient outcomes. The p53 pathway is a highly important regulatory process in a multitude of cell types, including embryonic, and the tumor suppressor gene TP53 is widely regarded as being one of the most important genes involved in tumorigenesis. Dysregulations in TP53 expression, along with altered expression of developmentally originating p53 regulators such as MDM2 and MDM4 have been implicated in various cancers, leading to poorer prognosis. Epithelial–mesenchymal transition (EMT), the process allowing epithelial cells to undergo biochemical changes to mesenchymal phenotypes, also plays a vital role in the fate of both embryonic and neoplastic cells. Genes that regulate EMT such as Twist1, SOX9 and REX1 have been associated with an increased occurrence of EMT in cancer cells, leading to enhanced cell stemness, proliferation and metastasis. The class of RNA that does not encode for proteins, known as non-coding RNA, has been implicated in a variety of cellular processes and emerging research has shown that its dysregulation can lead to uncontrolled cell proliferation and differentiation. Genes that have been shown to play a role in this dysregulation include PIWIL1, LIN28A and LIN28B, and have been associated with poorer patient outcomes and more aggressive cancer subtypes. The identification of these developmentally regulated genes in tumorigenesis has proved to play an advantageous role in cancer diagnosis and prognosis, and has provided researchers with a multitude of new target mechanisms for novel chemotherapeutic research.

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Section: Epithelial Mesenchymal Transition (Emt)mentioning

confidence: 99%

“…EMT is involved in three primary processes [ 24 , 25 , 26 ]. The first is during embryonic gastrulation and organ development, known as Type 1 EMT, in which the primitive epithelium (epiblast) transitions into primary mesenchyme, giving rise to the mesoderm, endoderm and mobile neural crest cells.…”

Section: Epithelial Mesenchymal Transition (Emt)mentioning

confidence: 99%

The Developmental Origins of Cancer: A Review of the Genes Expressed in Embryonic Cells with Implications for Tumorigenesis

Balachandran

Narendran

2023

Genes

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“…Epithelial‐mesenchymal transition (EMT) is the process by which epithelial cells transform into mesenchymal cells and acquire migratory abilities 61 . Cancer cells undergo EMT, which create a favorable microenvironment for cancer development and metastasis, and the acquisition of EMT functionality is associated with resistance to radiotherapy and poor prognosis in multiple types of malignant tumors.…”

Section: Molecular Mechanisms Of Radioresistance In Cancermentioning

confidence: 99%

“…Epithelial‐mesenchymal transition (EMT) is the process by which epithelial cells transform into mesenchymal cells and acquire migratory abilities. 61 Cancer cells undergo EMT, which create a favorable microenvironment for cancer development and metastasis, and the acquisition of EMT functionality is associated with resistance to radiotherapy and poor prognosis in multiple types of malignant tumors. One of the characteristics of EMT is the loss of intercellular adhesion and decreased expression of E‐cadherin; this progressive decline is regulated by the zinc finger proteins Snail and Slug.…”

Section: Molecular Mechanisms Of Radioresistance In Cancermentioning

confidence: 99%

Molecular mechanisms of chemo‐ and radiotherapy resistance and the potential implications for cancer treatment

Liu

Zheng

Huang

et al. 2021

MedComm

186

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Cancer is a leading cause of death worldwide. Surgery is the primary treatment approach for cancer, but the survival rate is very low due to the rapid progression of the disease and presence of local and distant metastasis at diagnosis. Adjuvant chemotherapy and radiotherapy are important components of the multidisciplinary approaches for cancer treatment. However, resistance to radiotherapy and chemotherapy may result in treatment failure or even cancer recurrence. Radioresistance in cancer is often caused by the repair response to radiation‐induced DNA damage, cell cycle dysregulation, cancer stem cells (CSCs) resilience, and epithelial‐mesenchymal transition (EMT). Understanding the molecular alterations that lead to radioresistance may provide new diagnostic markers and therapeutic targets to improve radiotherapy efficacy. Patients who develop resistance to chemotherapy drugs cannot benefit from the cytotoxicity induced by the prescribed drug and will likely have a poor outcome with these treatments. Chemotherapy often shows a low response rate due to various drug resistance mechanisms. This review focuses on the molecular mechanisms of radioresistance and chemoresistance in cancer and discusses recent developments in therapeutic strategies targeting chemoradiotherapy resistance to improve treatment outcomes.

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“…Epithelial to mesenchymal transition (EMT) is an intricate developmental program that enables cancer cells to suppress their epithelial features and change into mesenchymal features that allow them to become mobile and migrate to other sites [ 49 ]. In tumors with BRCA1 mutations, the expression of several key EMT factors is altered.…”

Section: Brca1 and Epithelial To Mesenchymal Transitionmentioning

confidence: 99%

BRCA1 and Metastasis: Outcome of Defective DNA Repair

Krishnan

Patel

Hakem

2021

Cancers

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Heritable mutations in BRCA1 and BRCA2 genes are a major risk factor for breast and ovarian cancer. Inherited mutations in BRCA1 increase the risk of developing breast cancers by up to 72% and ovarian cancers by up to 69%, when compared to individuals with wild-type BRCA1. BRCA1 and BRCA2 (BRCA1/2) are both important for homologous recombination-mediated DNA repair. The link between BRCA1/2 mutations and high susceptibility to breast cancer is well established. However, the potential impact of BRCA1 mutation on the individual cell populations within a tumor microenvironment, and its relation to increased aggressiveness of cancer is not well understood. The objective of this review is to provide significant insights into the mechanisms by which BRCA1 mutations contribute to the metastatic and aggressive nature of the tumor cells.

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Epithelial-mesenchymal transition in cancer: An overview

Cited by 14 publications

References 66 publications

The Developmental Origins of Cancer: A Review of the Genes Expressed in Embryonic Cells with Implications for Tumorigenesis

The Developmental Origins of Cancer: A Review of the Genes Expressed in Embryonic Cells with Implications for Tumorigenesis

Molecular mechanisms of chemo‐ and radiotherapy resistance and the potential implications for cancer treatment

BRCA1 and Metastasis: Outcome of Defective DNA Repair

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