Cadherin-mediated cell-cell interactions in normal and cancer cells

Gloushankova, Natalia A.; Rubtsova, Svetlana N.; Zhitnyak, Irina Y.

doi:10.1080/21688370.2017.1356900

Cited by 118 publications

(100 citation statements)

References 147 publications

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“…resonant frequency and stiffness of the epidermis found in verrucous carcinoma, basal cell carcinoma, and actinic keratosis may reflect differences in cell-to-cell attachments as opposed to changes in the physical properties of individual cells. A recent review22 suggests that adherens junctions, in neoplastic cells, involved in cell-tocell attachments, exhibit transformed organization, regulation, and stability. Increased organization of adherens junctions may offer an explanation for the increased resonant frequency and stiffness of the epidermis in precancerous and cancerous lesions observed by VOCT.…”

mentioning

confidence: 99%

Comparative “virtual biopsies” of normal skin and skin lesions using vibrational optical coherence tomography

Silver

Shah

Richard³

et al. 2019

Skin Research and Technology

132

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Background Increased tissue stiffness (also termed modulus) has been shown to be a characteristic of potential tumor metastasis. Measured values of the stiffness of tumors and cancer cells are reported in the literature to increase compared to neighboring normal tissues. Yet the relationship between the mechanical properties of cells and the extracellular matrix has yet to be correlated with the histopathology of cancerous lesions. Materials and Methods We have developed a technique to do virtual biopsies of skin lesions by combining images made using optical coherence tomography with stiffness measurements made simultaneously using vibrational analysis. The technique is termed vibrational optical coherence tomography (VOCT). Results In this paper, we report that precancerous and cancerous lesions are characterized by changes in both the morphology and stiffness of the cellular components of the skin. The ratio of the peak heights that correspond to the epidermal (40‐60Hz) and dermal (140‐160 Hz) resonant frequencies appear to be different for benign and cancerous or precancerous lesions compared with normal skin and scar. Conclusions Cell‐to‐cell and epidermal‐to‐dermal interactions may be very important in evaluating the potential of skin lesions to become malignant. These interactions can be evaluated using VOCT, a new technique for performing “virtual biopsies” of skin lesions.

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mentioning

confidence: 99%

Comparative “virtual biopsies” of normal skin and skin lesions using vibrational optical coherence tomography

Silver

Shah

Richard³

et al. 2019

Skin Research and Technology

132

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“…Data from this study also demonstrated that PAK‐1 inhibition decreased the expression of E‐cadherin, CXCR‐4, and HCAM. E‐cadherin plays a crucial role in the epithelial adherens junctions, where several proteins interact, including α‐ and β‐catenin, to mediate the actin cytoskeleton . Inhibition of E‐cadherin expression is required for EMT and plays a role in cancer migration and metastasis .…”

Section: Discussionmentioning

confidence: 99%

“…E-cadherin plays a crucial role in the epithelial adherens junctions, where several proteins interact, including α-and β-catenin, to mediate the actin cytoskeleton. 28 Inhibition of E-cadherin expression is required for EMT and plays a role in cancer migration and metastasis. 29 These data align with previous reports showing that PAK-1 regulates cytoskeletal organization and cell-cell interactions.…”

Section: Discussionmentioning

confidence: 99%

Effect of P21‐activated kinase 1 (PAK‐1) inhibition on cancer cell growth, migration, and invasion

Najahi‐Missaoui

Quach

Jenkins

et al. 2019

Pharmacology Res & Perspec

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P21‐activated kinase‐1 (PAK‐1) is a serine/threonine kinase involved in multiple signaling pathways that mediate cellular functions such as cytoskeletal motility, cell proliferation, and survival. PAK‐1 expression is altered in various cancers, including prostate and breast. Our recent studies showed that prostate cancer cells expressing higher levels of PAK‐1 were resistant to the cytotoxic effects of the PAK‐1 inhibitor, inhibitor targeting PAK‐1 activation‐3 (IPA‐3), compared to those with lower expression. This study expanded these findings to other cancers (breast and melanoma) by testing the hypothesis that genetic and pharmacological inhibition of PAK‐1 alters cell growth, migration, and invasion in prostate, breast, and skin cancer cell lines. We also tested the specificity of IPA‐3 for PAK‐1 and the hypothesis that gene silencing of PAK‐1 altered the efficacy of sterically stabilized liposomes (SSL) containing IPA‐3 (SSL‐IPA‐3). PAK‐1 expression was identified in four different breast cancer cell lines, and in a melanoma cell line. The expression of PAK‐1 correlated to the IC 50 of IPA‐3 as measured by MTT staining. PAK‐1 inhibition using shRNA correlated with decreased cell migration and invasion in prostate cancer DU‐145 and breast cancer MCF‐7 cells. Decreased migration and invasion also correlated to decreased expression of E‐cadherin and alterations in C‐X‐C Chemokine Receptor type 4 and Homing Cell Adhesion Molecule expression. PAK‐1 inhibition increased the cytotoxicity of IPA‐3, and the cytotoxicity of SSL‐IPA‐3 to levels comparable to that of free drug. These data demonstrate that both pharmacological and molecular inhibition of PAK‐1 decreased growth in prostate, breast, and melanoma cancer cell lines, and increased the toxicity of IPA‐3 and its liposomal formulation. These data also show the specificity of IPA‐3 for PAK‐1, are some of the first data suggesting that IPA‐3 is a therapeutic treatment for breast cancer and melanoma, and demonstrate the efficacy of liposome‐encapsulated IPA‐3 in breast cancer cells.

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“…To study the role of K19 on processes fundamental to metastasis, we examined the luminalsubtype MCF7 breast cancer cell line which expresses high levels of K19 27,28 . MCF7 cells maintain polarized epithelial phenotype with intact cell-cell adhesions made of desmosomes and adherens junctions [29][30][31] . Using MCF7 cells with complete ablation of K19 32 and KRT19 knockout (KO) cells with re-expression of K19, we observed that K19 is required for the epithelial-like cell shape and proper cell-cell adhesion.…”

Section: Introductionmentioning

confidence: 99%

Keratin 19 maintains E-cadherin localization at the cell surface and stabilizes cell-cell adhesion of MCF7 cells

Alsharif

Sharma

Bursch

et al. 2020

Preprint

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A cytoskeletal protein keratin 19 (K19) is highly expressed in breast cancer but its effects on breast cancer cell mechanics are unclear. Using KRT19 knockout (KO) cells and cells where K19 expression was rescued, we found that K19 is required to maintain rounded epithelial-like shape and tight cell-cell adhesion of MCF7 cells. A loss of K19 resulted in a lower level of plakoglobin and internalization of E-cadherin in early and recycling endosomes. Inhibiting internalization restored cell-cell adhesion of KRT19 KO cells, suggesting E-cadherin internalization contributes to defective adhesion. Ultimately, while K19 inhibited cell migration, it was required for cells to form colonies in suspension. Our results suggest that K19 stabilizes E-cadherin complexes at the cell membrane to maintain cell-cell adhesion which inhibits cell migration but provides growth and survival advantages for circulating tumor cells. These findings provide context-dependent roles of K19 during metastasis.

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Cadherin-mediated cell-cell interactions in normal and cancer cells

Cited by 118 publications

References 147 publications

Comparative “virtual biopsies” of normal skin and skin lesions using vibrational optical coherence tomography

Comparative “virtual biopsies” of normal skin and skin lesions using vibrational optical coherence tomography

Effect of P21‐activated kinase 1 (PAK‐1) inhibition on cancer cell growth, migration, and invasion

Keratin 19 maintains E-cadherin localization at the cell surface and stabilizes cell-cell adhesion of MCF7 cells

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