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Biology subjects

Sanjiv, K.

Publications and source records attributed to Sanjiv, K..

3 recordsLinked to original sources

A modular lentiviral system for multiplexed gene perturbation and functional analysis reveals interdependence of hormone receptors in breast cancer growth in vivo

Precise and flexible control of gene expression is essential for dissecting gene function in complex biological systems. Although recent developments in genetic engineering and CRISPR/Cas9 technology have expanded tools for gene activation, suppression and editing, their application in physiologically relevant models remains challenging, time consuming, and expensive. Here, we present a modular, doxycycline-inducible vector system that integrates gene overexpression, shRNA-mediated knockdown, and CRISPR/Cas9-mediated regulation within a single, lentivirus-compatible system. The modular design allows rapid exchange of selection markers, epitope tags, and reporters via Gateway cloning, providing broad adaptability across experimental settings. In addition to standard fluorescent and luminescent reporters, the system includes advanced sensors, such as Fucci cell cycle reporters, to enable monitoring of cellular processes. By combining fluorescence barcoding with combinatorial genetic perturbations, the platform supports multiplexed analysis of gene function and genetic interactions through phenotypic characterization by fluorescence imaging or flow cytometry. We demonstrate its utility in vivo with breast cancer intraductal xenografts, which suggest that ER+ breast cancer cells (MCF7) rely on androgen (AR), estrogen (ER) and progesterone receptors (PR) for in vivo growth. This versatile gene perturbation system provides tight temporal control, streamlined implementation, and high-content phenotyping capacity facilitating efficient in vitro and in vivo studies while reducing the use of animals in in vivo validation experiments. It thus expands the experimental repertoire for dynamic, multigene interrogation in complex systems.

molecular biology↗

Coupling cellular drug-target engagement to downstream pharmacology with CeTEAM

Cellular target engagement technologies are reforming drug discovery by enabling quantification of intracellular drug binding; however, simultaneous assessment of drug-associated phenotypes has proven challenging. CeTEAM (cellular target engagement by accumulation of mutant) is a platform that can concomitantly evaluate drug-target interactions and phenotypic responses for holistic assessment of drug pharmacology using conditionally-stabilized drug biosensors. We observe that drug-responsive proteotypes are prevalent among reported mutants of known drug targets. CeTEAM-compatible mutants follow structural and biophysical logic that permits intra-protein and paralogous expansion of the biosensor pool, as exemplified by alanine scanning of leucines within the PARP1 helical domain and transfer of PARP1 destabilization to the analogous PARP2 residue. We then apply CeTEAM to uncouple target engagement from divergent cellular activities of MTH1 inhibitors, dissect NUDT15-associated thiopurine metabolism with the R139C pharmacogenetic variant, and profile the live-cell dynamics of PARP1/2 binding and DNA trapping by PARP inhibitors. Further, PARP1-derived biosensors facilitated high-throughput screening of drug-like libraries for PARP1 binders, as well as multimodal ex vivo analysis and non-invasive tracking of PARPi binding in live animals. Our data suggests that CeTEAM can facilitate real-time, comprehensive characterization of target engagement by bridging drug binding events and their biological consequences.

biochemistry↗

MTH1 promotes mitotic progression to avoid oxidative DNA damage in cancer cells

BACKGROUNDWe developed MTH1 inhibitors (MTH1i) TH588 and TH1579 showing broad anti-cancer activity, while structurally distinct MTH1i fail to kill cancer cells. Here, we describe a new role of MTH1 in mitosis and the detailed mechanism of action of TH1579 (karonudib) and other structurally distinct MTH1i.\n\nMATERIALS AND METHODSCancer cell lines or zebrafish embryos were treated with MTH1i or siRNA targeting MTH1 and analysed primarily by live cell and immunofluorescence microscopy, survival assays, DNA fibre or COMET assays. MTH1 and tubulin interactions were analysed in vitro using co-immunoprecipitation and tubulin polymerisation assays.\n\nRESULTSHere, we describe a mitotic role for the MTH1 protein, which binds to tubulin, is required for microtubule polymerisation, correct spindle assembly, mitosis progression and suppression reactive oxygen species (ROS) generation in mitosis. Potent MTH1i display differential abilities to break the MTH1-tubulin interaction and cause mitotic arrest, demonstrating 8-oxodGTPase and mitotic function of MTH1 are mechanistically distinct. TH588 and TH1579 have more profound effect on mitotic arrest than other MTH1i explained by additional direct inhibition of tubulin polymerisation. MTH1i only inhibiting 8-oxodGTPase activity synergize with mitotic poisons.\n\nCONCLUSIONSEfficient MTH1 have a dual mechanism of action: inhibiting mitosis (to generate ROS) and promoting 8-oxodGTP incorporation into DNA during mitotic replication, dependent on ROS generation. Direct inhibition of tubulin polymerisation of TH588 and TH1579 increase their ability to arrest cells and generate ROS in mitosis. Furthermore, non-cytotoxic MTH1 can become effective and increase incorporation of oxidised nucleotides into DNA when combined with sub-therapeutic concentrations of mitotic inhibitors or challenged directly by 8-oxodGTP.

cancer biology↗