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Malignant Mesothelioma - BioProject

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Last Updated: 23 July 2022

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Human malignant mesothelioma NCI-H226 cells treated with TEAD inhibitor K-975 in SCID mice.

In vivo, we investigate the link between human malignant mesothelioma and gene TEAD transcription factors in order to maintain fully developed tumors. In vivo, TEAD inhibitor K-975 blocks tumor formation, ultimately leading to tumor formation, by downregulating TEAD gene expression and, thereby, TEAD-dependent transcription in a dysfunctional Hippo genetic background.

Source link: https://www.ncbi.nlm.nih.gov/bioproject/806971


Pharmacodynamics of malignant mesothelioma MSTO-211H dn-TEAD2 xenograft recurrence.

To maintain completely established tumors in vivo, we investigate the relationship of human malignant pleural mesothelioma on a complex YAP1-TEAD transcription factor complex. We show that expression of a doxycycline-dependent dominant negative TEAD2 temporarily alters YAP1/TEAD-dependent gene expression and reduces the proliferation of established tumor xenografts in a dysfunctional Hippo genetic background. TEAD-dependent transcription similar to untreated tumors is responsible for tumor growth regrowth, and TEAD-dependent transcription is re-activated, facilitating TEAD transcription complexes. The MSTO-211H cells, which were inoculated subcutaneously in mice and increased to about 300 mm3 under glucose supplementation, were inoculated in mice and remained to about 300 mm3 under glucose supplementation.

Source link: https://www.ncbi.nlm.nih.gov/bioproject/806953


Conditional expression of a dominant negative-TEAD2 construct modulates YAP1/TEAD-dependent transcription and arrests growth of human malignant mesothelioma MSTO-211H [TEAD2-dn] xenografts.

We demonstrate that expression of a common negative TEAD2 gene expression in a dysfunctional Hippo genetic background slows growth of established tumor xenografts. Our results show that TEAD2 participation is essential to maintain mesothelioma tumor formation in vivo in the context of a mutationated Hippo pathway, thus supporting the theory of limiting the triggered YAP1/TEAD complex for the treatment of malignant pleural mesothelioma patients. Human malignant mesothelioma MSTO-211H cells, which were inoculated subcutaneously in mice and allowed to grow to about 300 mm3 under glucose supplementation were inoculated to about 300 mm3 in mice.

Source link: https://www.ncbi.nlm.nih.gov/bioproject/806862


Conditional expression of sh-YAP1 modulates YAP1/TEAD-dependent transcription and causes regression of established human malignant mesothelioma MSTO-211H [sh-YAP1] xenografts.

We demonstrate that, in a dysfunctional Hippo genetic background, downregulation of YAP1 by shRNA results in modulation of YAP1/TEAD-dependent gene expression and regression of established tumor xenografts. Our results reveal that YAP1 activity is essential to maintain mesothelioma cells in vivo in the context of a mutationated Hippo pathway, thus supporting the theory of blocking the activated YAP1/TEAD complex for the treatment of malignant pleural mesothelioma patients. Overall layout: Malignant pleural mesothelioma MSTO-211H cells infected with a doxycycline-dependent sh-YAP1 construct were inoculated subcutaneously in mice and allowed to grow to about 300 mm3 under glucose supplementation.

Source link: https://www.ncbi.nlm.nih.gov/bioproject/806795

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions