RETRACTED ARTICLE: A83-01 inhibits TGF-β-induced upregulation of Wnt3 and epithelial to mesenchymal transition in HER2-overexpressing breast cancer cells

Wu, Yanyuan; Tran, Trinh; Dwabe, Sami; Sarkissyan, Marianna; Kim, Juri; Nava, Miguel; Clayton, Sheilah; Pietras, Richard J.; Farias‐Eisner, Robin; Vadgama, Jaydutt V.

doi:10.1007/s10549-017-4211-y

Cited by 47 publications

(34 citation statements)

References 41 publications

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“…Consistent with previous finding, we previously showed that the combination of RAGE-S100A8/A9 promoted the invasion and metastasis of breast cancer cells ( 8 ). Meanwhile, EMT regulated multiple signaling pathways, such as TGF-β ( 34 ), PI3K, MAPK, and Wnt/β-catenin. Numerous genes and transcription factors, such as Snail, Twist, and ZEB1/2 ( 35 , 36 ), have been found as key regulators in EMT.…”

Section: Discussionmentioning

confidence: 99%

miR‑185‑5p inhibits F‑actin polymerization and reverses epithelial mesenchymal transition of human breast cancer cells by modulating RAGE

et al. 2018

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In our previous study, advanced glycosylation end-product specific receptor (RAGE) was observed to bind to S100A8/A9 and cause epithelial mesenchymal transition (EMT). The results from target gene prediction revealed that microRNA (miR)-185-5p had a RAGE binding site. However, the function of miR-185-5p in the invasion and migration of breast cancer remains ambiguous. In the present study, the expression of miR-185-5p was examined in breast cancer tissues and cells. Clinical features revealed a negative correlation between miR-185-5p and tumor size, as well as in tumor differentiation and lymph node metastasis in breast cancer. In addition, miR-185-5p was negatively associated with RAGE, and this miRNA reversed the EMT of breast cancer by modulating RAGE in vitro. In addition, miR-185-5p inhibited the S100A8/A9-induced EMT of breast cancer cells by the nuclear factor-κB/Snail signaling pathway. Notably, miR-185-5p upregulation inhibited the F-actin polymerization induced by S100A8/A9 in breast cancer. Furthermore, overexpression of miR-185-5p and reduction of RAGE inhibited lung metastasis node in vivo. Thus, miR-185-5p represents a potential therapeutic target in breast cancer by modulating RAGE.

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Section: Discussionmentioning

confidence: 99%

miR‑185‑5p inhibits F‑actin polymerization and reverses epithelial mesenchymal transition of human breast cancer cells by modulating RAGE

et al. 2018

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“…The knockdown of Wnt3 in CRC cells suppressed the proliferation but enhanced the sensitivity to chemotherapeutics by inhibiting the canonical Wnt pathway and glycolytic pathway ( 90 ). A83-01 is a selective inhibitor of TGF-β receptor; it was shown to inhibit EMT in HER2-overexpressing breast cancer cells by interfering the TGF-β-induced upregulation of Wnt3 ( 91 ), whereas its application in treating CRC has not been reported.…”

Section: Roles Of Wnts In Tumorigenesis and The Progression Of Crcmentioning

confidence: 99%

Emerging Roles of Wnt Ligands in Human Colorectal Cancer

et al. 2020

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Colorectal cancer (CRC) is the fourth leading cause of cancer death worldwide, and constitutive activation of the Wnt signaling pathway is universal in most CRC cases. Wnt ligands (Wnts) are secreted glycoproteins and fundamentally essential for the transduction of Wnt signaling pathway. However, the 19 members of Wnts in humans imply a daunting complexity of Wnt signaling and biological effects, and our understanding of their roles in CRC tumorigenesis is still quite rudimentary. This review will give an overview of the structural characteristics and maturation process of Wnts. The expression pattern of all human Wnts in CRC tissues, including Wnt1, Wnt2,

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“…Inhibition of SKP1 leads to mitotic arrest of lung cancer cells [13]. Inhibitors of other activators of WNT signaling genes are being developed: PPP2CA [14], WNT3 [15] and others. For FZD2, on the contrary, it was shown that its hyperexpression was accompanied by suppression of metastasis of salivary adenoid cystic carcinomas [16].…”

Section: Laboratory and Experimental Studiesmentioning

confidence: 99%

Association of the Combination of Stemness Gene Amplifications and Copy Number Aberrations of WNT-Signaling Genes in Breast Tumors With Metastasis

et al. 2020

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We studied the association between the presence of 2 or more stemness gene amplifications as well as copy number aberrations (CNAs) of WNT signaling genes in residual breast tumor and metastasis. WNT pathway genes associated with metastasis were identified.Material and Methods. The study included 30 patients with breast cancer, who had 2 or more stemness gene amplifications in the residual tumor after neoadjuvant chemotherapy. Fifteen of the thirty patients developed hematogenous metastases; they constituted a group with metastases, the remaining 15 patients entered the second group without metastases. The tumor DNA was examined using a CytoScanHD Array microarray (Affymetrix, USA).Results. By subtracting amplification and deletion frequencies in 852 cytobands between groups with metastases and without metastases, 21 cytobands were identified with the largest difference in deletion and amplification frequencies. They contain 19/150 of WNT genes (12 activators: SKP1, WNT8A, MAPK9, CCND3, FZD9, WNT8B, CCND1, PLCB2, PRKCB, FZD2, WNT3, WNT9B and 7 negative regulators: GSK3B, APC, CSNK2B, SFRP5, BTRC, TCF7L2, CSNK2A2). A point system was developed: when amplifying WNT-signaling activators or deletion of negative regulators, one point was added to the total score, and vice versa when deleting WNT-signaling activators or amplification of negative regulators, one point was taken from the total amount. It was shown that 93% (14/15) of patients with metastases had a total score higher than 0, while 93% (14/15) of patients without metastases had a total score of zero or less than zero. The differences between the groups were statistically significant according to the two-sided Fisher test with a high level of confidence probability (p=0.000003) and the log-rank test (p=0.00004) when assessing non-metastatic survival by the Kaplan-Mayer method.Conclusion. Nineteen WNT signaling genes were identified. Copy number aberrations of these genes in combination with stemness gene amplifications in residual tumors were associated with metastasis. A new highly effective prognostic factor for breast cancer was identified.

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RETRACTED ARTICLE: A83-01 inhibits TGF-β-induced upregulation of Wnt3 and epithelial to mesenchymal transition in HER2-overexpressing breast cancer cells

Cited by 47 publications

References 41 publications

miR‑185‑5p inhibits F‑actin polymerization and reverses epithelial mesenchymal transition of human breast cancer cells by modulating RAGE

miR‑185‑5p inhibits F‑actin polymerization and reverses epithelial mesenchymal transition of human breast cancer cells by modulating RAGE

Emerging Roles of Wnt Ligands in Human Colorectal Cancer

Association of the Combination of Stemness Gene Amplifications and Copy Number Aberrations of WNT-Signaling Genes in Breast Tumors With Metastasis

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