Studying Interrelation of PDLIM4 with the Model of CD74-Mediated Development of Breast Cancer

Kravchenko, D. S.; Lezhnin, Yuriy Nikolaevich; Ivanova, Angelina; Kravchenko, Yulia Evgenyevna; Frolova, Elena I.

doi:10.3844/ojbsci.2017.50.57

Cited by 1 publication

(2 citation statements)

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“…This assumption is consistent with the results of our previous study, which revealed that RIL overexpression correlated with the unfavorable prognostic parameters of tumors, namely an increased CD74 level, reduced expression of E-cadherin, and inactivated intracellular tumor suppressor protein Scribble. Although the RILdependent mechanisms of tumor formation remain elusive, RIL may be involved in breast cancer development through the CD74-mediated mechanism typical of malignant cells [16] where increased expression of CD74 could lead to a mislocalization and inactivation of Scribble and loss of E-cadherin.…”

Section: Discussionmentioning

confidence: 99%

“…Conversely, a growing body of data suggests that RIL may also act as an oncogene [16][17][18]. The most aggressive breast cancer cell lines MDA-MB-231, MDA-MB-436, and BT-474 have high levels of RIL expression concomitant with unfavorable prognostic parameters, such as the increased CD74 and low E-cadherin levels [16]. These effects are not explained by the RIL-mediated attenuation of Src activity and call into question whether this model it universally applicable.…”

Section: Introductionmentioning

confidence: 99%

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PDLIM4/RIL-mediated regulation of Src and malignant properties of breast cancer cells

et al. 2020

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RIL/PDLIM4 gene was identified as a tumor suppressor, its expression is frequently altered in various types of malignancies. The product of RIL/PDLIM4 gene is an adapter protein involved in the actin cytoskeleton remolding and assembly of stress fibers crucial for cell motility and epithelial-mesenchymal transition. Although the exact mechanism tethering RIL to cancer development remains unknown some pieces of evidence suggest that RIL may act by suppressing activation of the protooncogene tyrosine-protein kinase Src. To further explore this issue we tested how different expression levels of RIL affected the activity of Src in breast cancer cell lines. RIL was ectopically overexpressed in the cell cultures with its relatively low endogenous level, or, otherwise, was downregulated by RNA interference. Whereas we observed no correlation between expression levels of RIL and activity of Src we found that in several cell lines elevated levels of RIL were associated with higher cell migratory activity along with the increased incidence of breast xenograft formation and metastasizing. The obtained data suggest that in some breast cancer models RIL may not act as Src kinase inhibitor, but rather play the role of a potential oncogene that promotes cell motility and contributes to cancer cells spreading.

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Section: Discussionmentioning

confidence: 99%