Monospecific antibody targeting of CDH11 inhibits epithelial-to-mesenchymal transition and represses cancer stem cell-like phenotype by up-regulating miR-335 in metastatic breast cancer, in vitro and in vivo

Chen, J.-H.

doi:10.1093/annonc/mdz268.070

Cited by 5 publications

(6 citation statements)

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“…Hence, Luan et al and Gu et al used miR-129-5p and miR-532-3p mimics, respectively, to enhance the chemosensitivity in vivo [118,119]. Recently, miR-147, miR-335, miR-1976, and miR-4319 were identified as tumor suppressor miRNAs for inhibiting EMT and CSCs simultaneously [120][121][122][123]. However, their roles in reversing drug resistance have not been demonstrated clearly, which need to be further explored.…”

Section: Mirnas Inhibit Cscs To Overcome Chemotherapy Resistancementioning

confidence: 99%

MiRNA-mediated EMT and CSCs in cancer chemoresistance

Dong

Zhu

et al. 2021

Exp Hematol Oncol

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Cancer stem cells (CSCs) are a small group of cancer cells, which contribute to tumorigenesis and cancer progression. Cancer cells undergoing epithelial-to-mesenchymal transition (EMT) acquire the chemoresistant ability, which is regarded as an important feature of CSCs. Thus, there emerges an opinion that the generation of CSCs is considered to be driven by EMT. In this complex process, microRNAs (miRNAs) are found to play a key role. In order to overcome the drug resistance, inhibiting EMT as well as CSCs phenotype seem feasible. Thereinto, regulating the EMT- or CSCs-associated miRNAs is a crucial approach. Herein, we conduct this review to elaborate on the complicated interplay between EMT and CSCs in cancer chemoresistance, which is modulated by miRNAs. In addition, we elucidate the therapeutic strategy to overcome drug resistance through targeting EMT and CSCs.

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Section: Mirnas Inhibit Cscs To Overcome Chemotherapy Resistancementioning

confidence: 99%

MiRNA-mediated EMT and CSCs in cancer chemoresistance

Dong

Zhu

et al. 2021

Exp Hematol Oncol

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“…In cancers, previous studies have shown that knockout of CDH11 gene can reduce the size of the formed mammary bulb and inhibit breast cancer tumorigenesis [36]. Chen et al [37] treated human metastatic breast cancer cell lines MCF7 and MDA-MB-231 with a single specific anti-CDH11 antibody mediated by miR-335, which proved that the antibody reduced the CD44 hi CD24 neg/lo cell population, inhibited the motility of breast cancer cells and the efficiency of mammary bulb formation. Lee et al [46] studied two kinds of antibodies, mAb 2C7 and 1A5, which blocked CDH11 mediated cell adhesion, and determined that the 343-348 motif of EC3 could be used as a good target for the treatment of CDH11 antibody.…”

Section: Discussionmentioning

confidence: 99%

“…CDH11 regulated the expression level of β-catenin, and played a key role in enhancing the stem cell, migration and invasion potential of TNBC cells by activating and regulating the typical Wnt-signaling pathway through the CDH11/β-catenin signal axis [36]. Chen et al [37] found that there was a negative correlation between CDH11 and MicroRNA-335 (miR-335), exposure to a single specific anti-CDH11 antibody could remarkably increase the ratio of miR-335/ CDH11, inhibit the expression of CDH11, β-catenin and vimentin, and inhibit the metastasis potential.…”

Section: Triple Negative Breast Cancer (Tnbc)mentioning

confidence: 99%

“…By targeting β-catenin and CDH11 to regulate the typical Wnt-signaling pathway and inhibit the cancer stem cell (CSC) like phenotype and metastasis phenotype of TNBC cells, it represents a new method of TNBC treatment, which provides a basis for further exploring CDH11 as a candidate target of TNBC targeted treatment [36,37].…”

Section: Triple Negative Breast Cancer (Tnbc)mentioning

confidence: 99%

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Research progress in the role and mechanism of Cadherin-11 in different diseases

Chen¹,

Xiang²,

Yu³

et al. 2021

J. Cancer

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Cadherin is an important cell-cell adhesion molecule, which mediates intercellular adhesion through calcium dependent affinity interaction. Cadherin-11 (CDH11, OB-cadherin) is a member of cadherin family, and its gene is situated on chromosome 16q22.1. Increasing lines of researches have proved that CDH11 plays important roles in the occurrence and development of a lot of diseases, such as tumors, arthritis and so on. CDH11 often leads to promoter methylation inactivation, which can induce cancer cell apoptosis, suppress cell motility and invasion, and can inhibit cancer through Wnt/β-catenin, AKT/Rho A and NF-κB signaling pathways. This review focused on the current knowledge of CDH11, including its function and mechanism in different diseases. In this article, we aimed to have a more comprehensive and in-depth understanding of CDH11 and to provide new ideas for the treatment of some diseases.

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“…CSCs are gradually becoming a new focus for exploring treatment strategies for tumor metastasis. To facilitate tumor progression, some CSCs undergo EMT to acquire the capacity to permeate through surrounding tissues and induce invasion and metastasis, suggesting that EMT is required for invasion and metastasis [48][49][50]. STAT3 activation causes changes in the expression of EMT marker proteins, indicating that STAT3 signaling may play an important part in the process of EMT [51].…”

Section: Discussionmentioning

confidence: 99%

Dihydroartemisinin Prevents Distant Metastasis of Laryngeal Carcinoma by Inactivating STAT3 in Cancer Stem Cells

Wang

Sun

et al. 2020

Med Sci Monit

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Background:Accumulating evidence indicates that cancer stem cells (CSCs) are a minor subpopulation of cancer cells that may be the primary source of cancer invasion, migration, and widespread metastasis. Material/Methods:We investigated the effects of dihydroartemisinin (DHA) on distant metastasis of laryngeal carcinoma and the relevant mechanism. In vitro, we used the Hep-2 human laryngeal squamous carcinoma cell line (Hep-2 cells) to assemble CSCs, using CD133 as the cell surface marker. Our data demonstrate that the CD133 + subpopulation of Hep-2 cells has greater invasion and migration capabilities than CD133cells. We also evaluated the effects of DHA, a newly defined STAT3 inhibitor, on the invasion and migration of CD133 + Hep-2 cells under hypoxia and IL-6 stimulation, both of which can activate STAT3 phosphorylation. Results:CSCs exhibited a significant decrease in the ability of migration and invasion upon the application of DHA, along with simultaneous alterations in related proteins, both in cultured cells and in xenograft tumors. The associated signaling proteins included phosphorylated STAT3 (p-STAT3), matrix metalloproteinase-9 (MMP-9), and E-cadherin, which are closely involved in cancer invasion and metastasis. In vivo, we found that DHA can reduce lung metastasis formation caused by CSCs and prolong survival in mice, and can inhibit STAT3 activation, downregulate MMP-9, and upregulate E-cadherin in lung metastatic tumors. Conclusions:Taken together, our findings indicate that CSCs possess stronger invasive and metastatic capabilities than non-CSCs, and DHA inhibits invasion and prevents metastasis induced by CSCs by inhibiting STAT3 activation.

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Monospecific antibody targeting of CDH11 inhibits epithelial-to-mesenchymal transition and represses cancer stem cell-like phenotype by up-regulating miR-335 in metastatic breast cancer, in vitro and in vivo

Cited by 5 publications

References 0 publications

MiRNA-mediated EMT and CSCs in cancer chemoresistance

MiRNA-mediated EMT and CSCs in cancer chemoresistance

Research progress in the role and mechanism of Cadherin-11 in different diseases

Dihydroartemisinin Prevents Distant Metastasis of Laryngeal Carcinoma by Inactivating STAT3 in Cancer Stem Cells

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