mProX™ Human CLDN6 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
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Published Data
Fig.1 The malignant phenotypes of MDA-MB-231 cells are subdued through the augmentation of CLDN6 expression.
The effect of cell growth was investigated using the growth curve, with a focus on how cell growth was impacted by CLDN6 overexpression, resulting in the inhibition of cell growth.
Ref: Yang, Minlan, et al. "CLDN6 enhances chemoresistance to ADM via AF-6/ERKs pathway in TNBC cell line MDAMB231." Molecular and Cellular Biochemistry 443 (2018): 169-180.
Pubmed: 29159771
DOI: 10.1007/s11010-017-3221-8
Research Highlights
Coy, Shannon. et al. "Systematic Characterization of Antibody-Drug Conjugate Targets in Central Nervous System Tumors." Neuro-oncology, 2023.
Antibody-drug conjugates (ADCs) have been developed to increase the specificity and efficacy of cytotoxic drugs, by directing them towards cells expressing specific target antigens. Numerous ADCs have been approved by the FDA for the treatment of solid and hematologic malignancies, such as those expressing HER2, TROP2, and NECTIN4. In recent studies, a specific ADC targeting HER2 (Trastuzumab-Deruxtecan) has demonstrated promising results by improving survival and reducing growth of brain metastases in treatment-resistant metastatic breast cancer, even in tumors with low HER2 expression. These findings suggest that even minimal levels of ADC target expression may still result in treatment responsiveness. However, the expression of ADC targets in central nervous system (CNS) tumors remains poorly characterized.
Coy, Shannon. et al. "Systematic Characterization of Antibody-Drug Conjugate Targets in Central Nervous System Tumors." Neuro-oncology, 2023.
Pubmed:
37870091
DOI:
10.1093/neuonc/noad205
Dong, Yuan. et al. "CLDN6 inhibits colorectal cancer proliferation dependent on restraining p53 ubiquitination via ZO-1/PTEN axis." Cellular signalling, 2023.
Colorectal cancer (CRC) is one of the most prevalent forms of cancer worldwide. The primary characteristic of cancer, abnormal cell proliferation, is responsible for the progression of CRC. CLDN6, an important component of tight junctions, has been shown to regulate proliferation in various tumors. Past research has demonstrated that low expression of CLDN6 is linked to CRC, and that overexpression of CLDN6 inhibits its proliferation. However, the full mechanism by which CLDN6 functions remains unclear. This study aims to investigate the association between CLDN6 and clinical features, as well as its molecular role in suppressing CRC proliferation. Our findings indicate a correlation between low CLDN6 expression and CRC grade and prognosis, and further reveal that CLDN6 impedes proliferation through the p53 pathway. Specifically, we have elucidated that CLDN6 regulates ubiquitination to enhance p53 stability and nuclear import through the PTEN/AKT/MDM2 pathway. Our data additionally suggests that CLDN6 binds to ZO-1 via its PDZ-binding motif (PBM), and interacts with PTEN to regulate the AKT/MDM2 pathway. Altogether, our study contributes to the understanding of CLDN6 as a potential biomarker for CRC diagnosis, treatment, and prognosis.
Dong, Yuan. et al. "CLDN6 inhibits colorectal cancer proliferation dependent on restraining p53 ubiquitination via ZO-1/PTEN axis." Cellular signalling, 2023.
Pubmed:
37852424
DOI:
10.1016/j.cellsig.2023.110930