Biology subjects

Mohammad, K.

Publications and source records attributed to Mohammad, K..

3 recordsLinked to original sources

bioRxiv2022

Epigenetic memory acquired during long-term EMTinduction governs the recovery to the epithelial state

Epithelial-Mesenchymal Transition (EMT) and its reverse Mesenchymal-Epithelial Transition (MET) are critical during embryonic development, wound healing and cancer metastasis. While phenotypic changes during short-term EMT induction are reversible, long-term EMT induction has been often associated with irreversibility. Here, we show that phenotypic changes seen in MCF10A cells upon long-term EMT induction by TGF{beta} need not be irreversible, but have relatively longer timescales of reversibility than those seen in short-term induction. Next, using a phenomenological mathematical model incorporating the epigenetic silencing of miR-200 by ZEB, we highlight how the epigenetic memory gained during long-term EMT induction can slow the recovery to the epithelial state post-TGF{beta} withdrawal. Our results suggest that epigenetic modifiers can govern the extent and timescale of EMT reversibility, and advise caution against labelling phenotypic changes seen in long-term EMT induction as irreversible.

cancer biology↗

bioRxiv2021

Rewiring the Three-Carbon Metabolism Abrogates Multiple MAPK-Induced Cellular Dysfunctions During Metabolic Disorder

Withdrawal noticeThe authors have withdrawn their manuscript. The lipidomic data presented in the manuscript were based on an excel summary sheet provided by VIT, whose group (AP and KM) conducted the analysis using an Orbitrap mass spectrometer. However, after submitting to BioRxiv, the VIT group could not recover the RAW (primary source) files from the lipidomic platform because these files were deleted due to the maintenance protocol used for the Orbitrap mass spectrometer. It was agreed to reconduct the lipidomic analysis. As the Orbitrap mass spectrometer was out of service at that time, the lipidomic analysis was conducted with the help of a QToF mass spectrometer. Important differences were noted for the relative abundance and species of many lipids across the strains compared to the previously reported data hence casting some doubt on their interpretation. Therefore, until further analysis can be carried out the authors do not wish this work to be cited as reference for the project. If you have any questions, please contact the corresponding author.

cell biology↗

bioRxiv2019

Mechanical Suppression of Breast Cancer Cell Invasion and Paracrine Signaling Requires Nucleo-Cytoskeletal Connectivity

Exercise benefits the musculoskeletal system and reduces the effects of cancer. The beneficial effects of exercise are multifactorial, where metabolic changes and tissue adaptation influence outcomes. Mechanical signals, a principal component of exercise, are anabolic to the musculoskeletal system and restrict cancer progression. We examined the mechanisms through which cancer cells sense and respond to mechanical signals. Low-magnitude, high-frequency signals were applied to human breast cancer cells in the form of low-intensity vibration (LIV). LIV decreased invasion through matrix and impaired secretion of osteolytic factors PTHLH, IL-11, and RANKL. Furthermore, paracrine signals from mechanically stimulated cancer cells, reduced osteoclast differentiation resorptive capacity. Physically disconnecting the nucleus by knockdown of SUN1 and SUN2 impaired the ability of LIV to suppress invasion and production of osteolytic factors. LIV also increased cell stiffness; an effect dependent on an intact LINC complex. These data show that mechanical signals alter the metastatic potential of human breast cancer cells, where the nucleus serves as a mechanosensory apparatus to alter cell structure and intercellular signaling.

cancer biology↗