Rab11 collaborates E‐cadherin to promote collective cell migration and indicates a poor prognosis in colorectal carcinoma

Chung, Yuan‐Chiang; Wei, Wan‐Chen; Hung, Chia-Nung; Kuo, Jen-Fang; Hsu, Chih‐Ping; Chang, King‐Jen; Chao, Wei‐Ting

doi:10.1111/eci.12683

Cited by 39 publications

(23 citation statements)

References 44 publications

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“…The upregulation of CDH12 protein following DMH administration with the development of ACF is consistent with the fact that CDH12 promotes proliferation and tumorigenesis [46,47]. This In support, SOX7 over-expression suppressed cell proliferation and colony formation in prostate and CRC cell lines and induced apoptosis in CRC cells [49,50].…”

Section: Combination Treatment With Qu and 5-fu Was Associated With Dsupporting

confidence: 67%

Combination Therapy with Quercetin and 5-Fluorouracil Ameliorates 1,2-Dimethylhydrazine Induced Carcinogenesis in the Colon of Wistar Rats.

Elsadek

Aziz

El-Deek

et al. 2017

BESPS

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Background: Colorectal carcinoma (CRC) is a common cause of cancer-related death worldwide. 5-fluorouracil (5-FU), a first-line chemotherapeutic drug in CRC, has several side effects limiting its therapeutic outcomes. Quercetin (QU) is a dietary bioflavonoid with antioxidant and cytotoxic prooxidant properties. Here, we hypothesize that combination treatment with QU and 5-FU can modulate 1,2-dimethylhydrazine (DM H) induced histological and biochemical changes in the colon of Wistar rats. Methods: A Wistar rats CRC model was established and the animals were randomly d ivided into five groups. Rats in group A received a suspending vehicle . Group B rats received DMH t wice a week subcutaneously for 4 weeks. Animals in the other groups (C, D and E) received the same treatment of DMH, along with QU or 5 -FU (indiv idually) or combined QU+5-FU treat ment. Results: The DMH-treated rats developed adverse histological alterations (aberrant crypt foci, ACF) and biochemical changes (elevated serum CA19-9; reduced tissue levels of enzy mat ic antio xidants; elevated CDH12 p rotein expression and decreased SOX7 mRNA levels). Treat ment of DMH-treated animals with QU+5-FU (but not with QU or 5-FU, individually) significantly reversed these changes (i.e., suppressed the formation of ACF; decreased the CA19-9 levels; reduced CDH12 protein exp ression and increased SOX7 mRNA expression). Conclusions: Conclusively, to the best of our knowledge, our study was the first to evaluate the effects of QU+5-FU treat ment on the histological and molecu lar changes following DMH ad min istration in a rat colon model. Our data suggest that combination therapy with QU+5 -FU has therapeutic benefits in colon cancer induced by DMH, with potential for translation to spontaneous disease.

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Section: Combination Treatment With Qu and 5-fu Was Associated With Dsupporting

confidence: 67%

Combination Therapy with Quercetin and 5-Fluorouracil Ameliorates 1,2-Dimethylhydrazine Induced Carcinogenesis in the Colon of Wistar Rats.

Elsadek

Aziz

El-Deek

et al. 2017

BESPS

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“…Collective migration involving groups of cells, which is commonly seen at the borders of invasive carcinomas, is best documented in the case of carcinomas of the breast and lungs (Friedl et al, 2012); similar invasive cohorts undoubtedly participate in invasion by other types of carcinoma cells as well (Chung et al, 2016; Veracini et al, 2015). Cells residing within these invasive cell phalanxes continue to express key epithelial markers such as E-cadherin, which helps to sustain the cohesion between the individual epithelial cells within these cohorts.…”

Section: Dissemination Of Carcinoma Cellsmentioning

confidence: 99%

Emerging Biological Principles of Metastasis

Lambert

Pattabiraman

Weinberg

2017

Cell

2,470

2,160

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Metastases account for the great majority of cancer-associated deaths, yet this complex process remains the least understood aspect of cancer biology. As the body of research concerning metastasis continues to grow at a rapid rate, the biological programs that underlie the dissemination and metastatic outgrowth of cancer cells are beginning to come into view. In this review we summarize the cellular and molecular mechanisms involved in metastasis, with a focus on carcinomas where the most is known, and highlight the general principles of metastasis that have begun to emerge.

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“…Alternatively, tumor cells display a faster movement via so-called amoeboid cell invasion. By contrast, leader cells of collectively migrating cancer cells exhibit a mesenchymal migration phenotype whereby inner cells of the collectively migrating unit retain their epithelial phenotype [3, 38]. …”

Section: Introductionmentioning

confidence: 99%

Breast Carcinoma: From Initial Tumor Cell Detachment to Settlement at Secondary Sites

Melzer

Ohe

Hass

2017

BioMed Research International

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Metastasis represents a multistep cascade of cancer cell alterations accompanied by structural and functional changes within the tumor microenvironment which may involve the induction of a retrodifferentiation program. Major steps in metastatic developments include (A) cell detachment from the primary tumor site involving epithelial-mesenchymal transition (EMT), (B) migration and invasion into surrounding tissue, (C) transendothelial intravasation into the vasculature of blood and/or lymphatic vessels as circulating tumor cells (CTCs), (D) dissemination to distant organs, and (E) extravasation of CTCs to secondary sites as disseminated tumor cells (DTCs). This article highlights some aspects of the metastatic cascade with a focus on breast cancer cells. Metastatic steps critically depend on the capability of cancer cells to adapt to distant tissues and the corresponding new microenvironment. As a consequence, increasing plasticity and developmental changes paralleled by acquisition of new cancer cell functionalities challenge a successful therapeutic approach.

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Rab11 collaborates E‐cadherin to promote collective cell migration and indicates a poor prognosis in colorectal carcinoma

Abstract: This study demonstrated that Rab11 and E-cadherin expressions are indicators of poor survival time in colorectal carcinoma, but that Rab11 overexpression may contribute to increased collective cell invasion in colorectal carcinoma.

Cited by 39 publications

References 44 publications

Combination Therapy with Quercetin and 5-Fluorouracil Ameliorates 1,2-Dimethylhydrazine Induced Carcinogenesis in the Colon of Wistar Rats.

Combination Therapy with Quercetin and 5-Fluorouracil Ameliorates 1,2-Dimethylhydrazine Induced Carcinogenesis in the Colon of Wistar Rats.

Emerging Biological Principles of Metastasis

Breast Carcinoma: From Initial Tumor Cell Detachment to Settlement at Secondary Sites

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