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Shahi, N.

Publications and source records attributed to Shahi, N..

3 recordsLinked to original sources

Neuromodulation of Swarming Behavior in C. elegans: Insights into the Conserved role of Calsyntenins

Collective animal behaviors arise from a complex interplay between internal physiological states and external environmental cues. In Caenorhabditis elegans, favorable conditions promote dispersal, while stressors like food scarcity or overcrowding trigger aggregation. Here, we describe a distinct behavior termed as swarming, where C. elegans move and feed in aggregates despite abundant food availability. While environmental factors have been implicated in this behavior, the underlying genetic and molecular mechanisms remain unclear. We identify a novel role for the conserved calsyntenin protein CASY-1 in regulating swarming. Through genetic, behavioral, and optogenetic approaches, we show that CASY-1 functions in sensory neurons to modulate the neuropeptide pigment-dispersing factor (PDF) signaling. Mutants in casy-1 show impaired PDF-1 signaling and reduced inhibition of the serotonin pathway, a known regulator of social behaviors. This dysregulation, along with its associated mechanosensory and foraging defects, likely contributes to the swarming phenotype. Our findings reveal a putative neuromodulatory pathway critical for swarming behavior in C. elegans.

neuroscience↗

Knockdown of CSNK2β suppresses MDA-MB231 cells growth, induces apoptosis, inhibits migration and invasion

Breast cancer is most common cancer among women worldwide and among different types of breast cancer treatment of triple-negative breast cancer is major challenge, thus identification of specific drivers is required for targeted therapies of this malignancy. The aim of the present study is to elucidate the effects of silencing of CSNK2{beta} gene by small interfering RNA (siRNA) on proliferation, cell cycle and apoptosis in breast carcinoma MDA MB-231 cells. Silencing of CSNK2{beta} in MDA-MB-231(a triple negative cell line) cells resulted in decreased cell viability and colony formation. Cell cycle analysis showed that silencing of CSNK2{beta} arrested MDA MB-231 cells in G2/M phase. We demonstrated that silencing of CSNK2{beta} promoted nuclear condensation and augmented intracellular ROS production. Furthermore, Silencing of CSNK2{beta} in MDA-MB 231 cells modulated the apoptotic machinery- BAX, Bcl-xL and caspase 3; autophagy machinary-Beclin-1 and LC3-1; and inhibited the vital markers (p-ERK, c-Myc, NF-{kappa}B, E2F1, PCNA, p38-) associated with cell proliferation and DNA replication pathways. In addition, Knocking down of CSNK2 {beta} also affected the migration potential of MDA-MB231 as observed in the wound healing and transwell migration assays. Together, our study suggests that CSNK2{beta} silencing may offer future therapeutic target in triple negative breast cancer.

cancer biology↗

Silencing of the CSNK2β gene by siRNA inhibits invasiveness and growth of MDA-MB-231 cells

BackgroundBreast cancer is most common cancer and accounts for one-fourth of all cancer diagnoses worldwide. Treatment of triple-negative breast cancer is major challenge and identification of specific drivers is required for targeted therapies. The aim of our present study is to elucidate the therapeutic potential of CSNK2{beta} silencing in triple negative breast cancer MDA-MB-231 cell.\n\nMethodsCSNK2{beta} gene has been knockdown using siRNA and silencing was estimated by both real time and western blot. Cell Titer-Glo (CTG) and colony formation assay and wound healing assay, cell cycle analysis by flow cytometry was performed to assess the role of CSNK2{beta} in cell proliferation, migration, cell cycle, and oncogenesis. Morphological assessment of nuclear condensation, apoptosis by Hoechst staining and measurement of intracellular ROS production was examined using fluorescence microscopy. Real time PCR and western blot was done to study the expression of genes related to cell proliferation, survival, metastasis, apoptosis, and autophagy.\n\nResultsSilencing of CSNK2{beta} in MDA-MB-231 cells resulted in decreased cell viability, colony formation, and migratory potential. Cell cycle analysis showed that growth inhibitory effect was mediated by arresting the cells in G2/M phase. Furthermore, we demonstrated that silencing of CSNK2{beta} increased the nuclear condensation and intracellular ROS production. CSNK2{beta} regulates the expression of BAX, Bcl-xL, caspase 3, Beclin-1, LC3-I, p-ERK, p38-, c-Myc, MAPK, c-Jun, NF-B, {beta}-catenin, E2F1, PCNA. We have also shown the functional relationship between CSNK2{beta}, PIN1, and PTOV1 by western blotting. We have first time reported that silencing CSNK2{beta} using siRNA can inhibit invasiveness and proliferation of MDA-MB-213 cells.\n\nConclusionOur results suggested that CSNK2{beta} silencing may offer future therapeutic target in triple negative breast cancer.

cancer biology↗