CLDN6 enhances chemoresistance to ADM via AF-6/ERKs pathway in TNBC cell line MDAMB231

Yang, Minlan; Li, Yanru; Ruan, Yuanyuan; Lü, Yan; Lin, Dongjing; Xie, Yinping; Dong, Bing; Dang, Qihua; Quan, Chengshi

doi:10.1007/s11010-017-3221-8

Cited by 29 publications

(26 citation statements)

References 37 publications

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“…Changes in CLDN gene expression were essentially seen in the CMS2 and CMS4 subtypes for which a clear distinction in sensitivity to chemotherapy-induced apoptosis has been reported 67. This suggests that in CRC, claudins could play a role in chemoresistance, as previously shown for CLDN4 and CLDN7 in ovarian cancer,68,69 and more recently, for CLDN6 in triple-negative breast cancer cells 70…”

Section: Discussionmentioning

confidence: 54%

<p>Claudin gene expression profiles and clinical value in colorectal tumors classified according to their molecular subtype</p>

Cherradi¹,

Martineau²,

Gongora³

et al. 2019

CMAR

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Purpose Colorectal cancer (CRC) is a heterogeneous disease that can be classified into distinct molecular subtypes. The aims of this study were 1) to compare claudin ( CLDN ) gene expression in CRC samples and normal colon mucosa, and then in the different CRC molecular subtypes, and 2) to assess their prognostic value. Patients and methods CLDN expression in CRC samples was analyzed using gene expression data for a cohort of 143 primary CRC samples, and compared in the same CRC samples classified into different molecular subtypes (C1 to C6 according to the Marisa’s classification, and CMS1 to CMS4 of the consensus classification). Comparison of CLDN expression in normal and tumor colon samples was also made on a smaller number of samples. Then, the relationship between CLDN expression profiles and overall survival (OS) and progression-free survival was examined. Results Compared with normal mucosa, CLDN1 and CLDN2 were upregulated, whereas CLDN5 , 7 , 8 , and 23 were downregulated in CRC samples. Variations in CLDN expression profiles were observed mainly in the CMS2/C1 and CMS4/C4 subtypes. Overall, expression of CLDN2 or CLDN4 alone had a strong prognostic value that increased when they were associated. In the CMS4/C4 subtypes, lower expressions of CLDN11 , CLDN12 , and CLDN23 were associated with longer OS. Conversely, in the CMS2 and C1 subtypes, low CLDN23 expression was associated with shorter OS and progression-free survival, suggesting a dual role for CLDN23 as a tumor suppressor/promoter in CRC. CLDN6 and CLDN11 had a prognostic value in the CMS2 and C4 subtypes, respectively. Conclusion This analysis of CLDN gene expression profiles and prognostic value in CRC samples classified according to their molecular subtype shows that CRC heterogeneity must be taken into account when assessing CLDN potential value as prognostic markers or therapeutic targets.

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Section: Discussionmentioning

confidence: 54%

<p>Claudin gene expression profiles and clinical value in colorectal tumors classified according to their molecular subtype</p>

Cherradi¹,

Martineau²,

Gongora³

et al. 2019

CMAR

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“…Interestingly, Afadin has been demonstrated recently to interact with Claudin-6 in MDA-MB-231 breast cancer cells. Claudin-6 colocalized and interacted with Afadin, resulting in suppression of ERK signaling, increased stem cell characteristics, and enhanced chemoresistance to adriamycin (Yang et al 2018).…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, Afadin has been shown to be important for heterotypic N-Cadherin/E-Cadherin interactions between cancer-associated fibroblasts and cancer cells that drive cellular invasion (Labernadie et al 2017). Afadin can also contribute to chemoresistance in TNBC cells through interactions with Claudin-6 and subsequent suppression of ERK signaling (Yang et al 2018). Roles for Afadin in modulating cell death and/or survival have also been reported.…”

Section: Discussionmentioning

confidence: 99%

Afadin cooperates with Claudin-2 to promote breast cancer metastasis

et al. 2019

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Claudin-2 promotes breast cancer liver metastasis by enabling seeding and early cancer cell survival. We now demonstrate that the PDZ-binding motif of Claudin-2 is necessary for anchorage-independent growth of cancer cells and is required for liver metastasis. Several PDZ domain-containing proteins were identified that interact with the PDZ-binding motif of Claudin-2 in liver metastatic breast cancer cells, including Afadin, Arhgap21, Pdlim2, Pdlim7, Rims2, Scrib, and ZO-1. We specifically examined the role of Afadin as a potential Claudin-2-interacting partner that promotes breast cancer liver metastasis. Afadin associates with Claudin-2, an interaction that requires the PDZbinding motif of Claudin-2. Loss of Afadin also impairs the ability of breast cancer cells to form colonies in soft agar and metastasize to the lungs or liver. Immunohistochemical analysis of Claudin-2 and/or Afadin expression in 206 metastatic breast cancer tumors revealed that high levels of both Claudin-2 and Afadin in primary tumors were associated with poor disease-specific survival, relapse-free survival, lung-specific relapse, and liver-specific relapse. Our findings indicate that signaling downstream from a Claudin-2/Afadin complex enables the efficient formation of breast cancer metastases. Moreover, combining Claudin-2 and Afadin as prognostic markers better predicts the potential of breast cancer to metastasize to soft tissues.

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“…In addition, research has shown that estrogen receptor β (ERβ) plays an anti-cancer role in breast cancer, and Song et al demonstrated that this effect is mediated by claudin-6 [106]. On the other hand, Yang et al demonstrated that claudin-6 affects chemo-resistance in MDA-MB-231 cells in response to adriamycin (ADM) by reducing the drug-induced apoptosis [107]. Previous studies reported that decreased expression of claudin-2 is associated with increasing stage of cancer and with lymph node metastasis [108,109].…”

Section: Claudins In Breast Cancermentioning

confidence: 99%

Claudins: New Players in Human Fertility and Reproductive System Cancers

Kozieł

Kowalska

Piastowska-Ciesielska

2020

Cancers

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Claudins are major integral proteins of tight junctions (TJs), the apical cell-cell adhesions that enable maintaining polarity of epithelial cells, their differentiation, and cell signaling. A number of studies have indicated that claudins might play a crucial role in both physiology and pathogenesis. Their tissue-specific expression was originally linked to the development of different types of cancer and triggered a hope to use them as diagnostic or prognostic markers. However, it seems that their expression is more complex than that, and undoubtedly, claudins participate in one of the most important molecular events in cells. This review summarizes the recent research evaluating the role of claudins in fertility and the most common endocrine-dependent cancers in the reproductive system and highlights the crucial role of claudins both in human fertility and the most common cancers.

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CLDN6 enhances chemoresistance to ADM via AF-6/ERKs pathway in TNBC cell line MDAMB231

Cited by 29 publications

References 37 publications

<p>Claudin gene expression profiles and clinical value in colorectal tumors classified according to their molecular subtype</p>

<p>Claudin gene expression profiles and clinical value in colorectal tumors classified according to their molecular subtype</p>

Afadin cooperates with Claudin-2 to promote breast cancer metastasis

Claudins: New Players in Human Fertility and Reproductive System Cancers

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