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34 results on '"Jolly, Mohit K."'

1. Spatio-temporal Pattern Formation due to Host-Circuit Interplay in Gene Expression Dynamics

Author

Chakraborty, Priya, Roy, Ushasi, Jolly, Mohit K., and Ghosh, Sayantari

Subjects
Quantitative Biology - Quantitative Methods, Nonlinear Sciences - Pattern Formation and Solitons
Abstract

Biological systems are majorly dependent on their property of bistability in order to exhibit nongenetic heterogeneity in terms of cellular morphology and physiology. Spatial patterns of phenotypically heterogeneous cells, arising due to underlying bistability, may play significant role in phenomena like biofilm development, adaptation, cell motility etc. While nonlinear positive feedback regulation, like cooperative heterodimer formation are the usual reason behind bistability, similar dynamics can also occur as a consequence of host-circuit interaction. In this paper, we have investigated the pattern formation by a motif with non-cooperative positive feedback, that imposes a metabolic burden on its host due to its expression. In a cellular array set inside diffusible environment, we investigate spatio-temporal diffusion in one dimension as well as in two dimension in the context of various initial conditions respectively. Moreover, the number of cells exhibiting the same steady state, as well as their spatial distribution has been quantified in terms of connected component analysis. The effect of diffusion coefficient variation has been studied in terms of stability of related states and time evolution of patterns., Comment: 33 pages, 11 figures

Published
2022
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2. Biophysical and Biochemical mechanisms underlying Collective Cell Migration in Cancer Metastasis

Author

Roy, Ushasi, Collins, Tyler, Jolly, Mohit K., and Katira, Parag

Subjects
Quantitative Biology - Cell Behavior, Physics - Biological Physics, Quantitative Biology - Quantitative Methods
Abstract

Multicellular collective migration is a ubiquitous strategy of cells to translocate spatially in diverse tissue environments to accomplish a wide variety of biological phenomena, viz. embryonic development, wound healing, and tumor progression. Diverse cellular functions and behaviors, for instance, cell protrusions, active contractions, cell-cell adhesion, biochemical signaling, remodeling of tissue micro-environment, etc., play their own role concomitantly to have a single concerted consequence of multicellular migration. Thus unveiling the driving principles, both biochemical and biophysical, of the inherently complex process of collective cell migration is an insurmountable task. Mathematical and computational models, in tandem with experimental data, help in shedding some light on it. Here we review different factors influencing Collective Cell Migration and then focus on different mathematical and computational models - discrete, hybrid, and continuum - which helps in revealing different aspects of multicellular migration. Finally, we discuss the applications of these modeling frameworks specific to cancer, Comment: 27 pages, 2 figures, book chapter

Published
2022

7. Distinct melanocyte subpopulations defined by stochastic expression of proliferation or maturation programs enable a rapid and sustainable pigmentation response.

Author

Aggarwal, Ayush, Nasreen, Ayesha, Sharma, Babita, Sahoo, Sarthak, Aswin, Keerthic, Faruq, Mohammed, Pandey, Rajesh, Jolly, Mohit K., Singh, Abhyudai, Gokhale, Rajesh S., and Natarajan, Vivek T.

Subjects
HUMAN skin color, GENE regulatory networks, HISTONE acetylation, GENE expression, CHROMATOPHORES
Abstract

The ultraviolet (UV) radiation triggers a pigmentation response in human skin, wherein, melanocytes rapidly activate divergent maturation and proliferation programs. Using single-cell sequencing, we demonstrate that these 2 programs are segregated in distinct subpopulations in melanocytes of human and zebrafish skin. The coexistence of these 2 cell states in cultured melanocytes suggests possible cell autonomy. Luria–Delbrück fluctuation test reveals that the initial establishment of these states is stochastic. Tracking of pigmenting cells ascertains that the stochastically acquired state is faithfully propagated in the progeny. A systemic approach combining single-cell multi-omics (RNA+ATAC) coupled to enhancer mapping with H3K27 acetylation successfully identified state-specific transcriptional networks. This comprehensive analysis led to the construction of a gene regulatory network (GRN) that under the influence of noise, establishes a bistable system of pigmentation and proliferation at the population level. This GRN recapitulates melanocyte behaviour in response to external cues that reinforce either of the states. Our work highlights that inherent stochasticity within melanocytes establishes dedicated states, and the mature state is sustained by selective enhancers mark through histone acetylation. While the initial cue triggers a proliferation response, the continued signal activates and maintains the pigmenting subpopulation via epigenetic imprinting. Thereby our study provides the basis of coexistence of distinct populations which ensures effective pigmentation response while preserving the self-renewal capacity. Ultraviolet (UV) radiation triggers a pigmentation response in human skin, wherein melanocytes rapidly activate divergent maturation and proliferation programs. Here, the authors identify distinct melanocyte sub-populations with maturation and proliferation programs initiated by stochastic gene expression in response to external pigmentation cues such as UV. [ABSTRACT FROM AUTHOR]

Published
2024
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8. Chronic Obstructive Pulmonary Disease and Lung Cancer: Underlying Pathophysiology and New Therapeutic Modalities

Author

Eapen, Mathew Suji, Hansbro, Philip M., Larsson‑Callerfelt, Anna-Karin, Jolly, Mohit K., Myers, Stephen, Sharma, Pawan, Jones, Bernadette, Rahman, Md Atiqur, Markos, James, Chia, Collin, Larby, Josie, Haug, Greg, Hardikar, Ashutosh, Weber, Heinrich C., Mabeza, George, Cavalheri, Vinicius, Khor, Yet H., McDonald, Christine F., and Sohal, Sukhwinder Singh

Published
2018
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10. Supplementary Table 1 from MCAM Mediates Chemoresistance in Small-Cell Lung Cancer via the PI3K/AKT/SOX2 Signaling Pathway

Author

Tripathi, Satyendra C., primary, Fahrmann, Johannes F., primary, Celiktas, Muge, primary, Aguilar, Mitzi, primary, Marini, Kieren D., primary, Jolly, Mohit K., primary, Katayama, Hiroyuki, primary, Wang, Hong, primary, Murage, Eunice N., primary, Dennison, Jennifer B., primary, Watkins, D. Neil, primary, Levine, Herbert, primary, Ostrin, Edwin J., primary, Taguchi, Ayumu, primary, and Hanash, Samir M., primary

Published
2023
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11. Data from MCAM Mediates Chemoresistance in Small-Cell Lung Cancer via the PI3K/AKT/SOX2 Signaling Pathway

Author

Tripathi, Satyendra C., primary, Fahrmann, Johannes F., primary, Celiktas, Muge, primary, Aguilar, Mitzi, primary, Marini, Kieren D., primary, Jolly, Mohit K., primary, Katayama, Hiroyuki, primary, Wang, Hong, primary, Murage, Eunice N., primary, Dennison, Jennifer B., primary, Watkins, D. Neil, primary, Levine, Herbert, primary, Ostrin, Edwin J., primary, Taguchi, Ayumu, primary, and Hanash, Samir M., primary

Published
2023
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12. Supplementary Table 2 from MCAM Mediates Chemoresistance in Small-Cell Lung Cancer via the PI3K/AKT/SOX2 Signaling Pathway

Author

Tripathi, Satyendra C., primary, Fahrmann, Johannes F., primary, Celiktas, Muge, primary, Aguilar, Mitzi, primary, Marini, Kieren D., primary, Jolly, Mohit K., primary, Katayama, Hiroyuki, primary, Wang, Hong, primary, Murage, Eunice N., primary, Dennison, Jennifer B., primary, Watkins, D. Neil, primary, Levine, Herbert, primary, Ostrin, Edwin J., primary, Taguchi, Ayumu, primary, and Hanash, Samir M., primary

Published
2023
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13. Supplementary Figures from MCAM Mediates Chemoresistance in Small-Cell Lung Cancer via the PI3K/AKT/SOX2 Signaling Pathway

Author

Tripathi, Satyendra C., primary, Fahrmann, Johannes F., primary, Celiktas, Muge, primary, Aguilar, Mitzi, primary, Marini, Kieren D., primary, Jolly, Mohit K., primary, Katayama, Hiroyuki, primary, Wang, Hong, primary, Murage, Eunice N., primary, Dennison, Jennifer B., primary, Watkins, D. Neil, primary, Levine, Herbert, primary, Ostrin, Edwin J., primary, Taguchi, Ayumu, primary, and Hanash, Samir M., primary

Published
2023
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14. Supplementary Data from MCAM Mediates Chemoresistance in Small-Cell Lung Cancer via the PI3K/AKT/SOX2 Signaling Pathway

Author

Tripathi, Satyendra C., primary, Fahrmann, Johannes F., primary, Celiktas, Muge, primary, Aguilar, Mitzi, primary, Marini, Kieren D., primary, Jolly, Mohit K., primary, Katayama, Hiroyuki, primary, Wang, Hong, primary, Murage, Eunice N., primary, Dennison, Jennifer B., primary, Watkins, D. Neil, primary, Levine, Herbert, primary, Ostrin, Edwin J., primary, Taguchi, Ayumu, primary, and Hanash, Samir M., primary

Published
2023
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22. Dynamic Phenotypic Switching and Group Behavior Help Cancer Cells Evade Chemotherapy

Author

Nam, Arin, primary, Mohanty, Atish, additional, Bhattacharya, Supriyo, additional, Kotnala, Sourabh, additional, Achuthan, Srisairam, additional, Hari, Kishore, additional, Srivastava, Saumya, additional, Guo, Linlin, additional, Nathan, Anusha, additional, Chatterjee, Rishov, additional, Rangarajan, Govindan, additional, Massarelli, Erminia, additional, Levine, Herbert, additional, Jolly, Mohit K., additional, Kulkarni, Prakash, additional, and Salgia, Ravi, additional

Published
2020
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24. An integrative systems biology and experimental approach identifies convergence of epithelial plasticity, metabolism, and autophagy to promote chemoresistance

Author

Xu, Shengnan, primary, Ware, Kathryn E., additional, Ding, Yuantong, additional, Kim, So Young, additional, Sheth, Maya, additional, Rao, Sneha, additional, Chan, Wesley, additional, Armstrong, Andrew J., additional, Eward, William C., additional, Jolly, Mohit K., additional, and Somarelli, Jason A., additional

Published
2018
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27. MCAM Mediates Chemoresistance in Small-Cell Lung Cancer via the PI3K/AKT/SOX2 Signaling Pathway

Author

Tripathi, Satyendra C., primary, Fahrmann, Johannes F., additional, Celiktas, Muge, additional, Aguilar, Mitzi, additional, Marini, Kieren D., additional, Jolly, Mohit K., additional, Katayama, Hiroyuki, additional, Wang, Hong, additional, Murage, Eunice N., additional, Dennison, Jennifer B., additional, Watkins, D. Neil, additional, Levine, Herbert, additional, Ostrin, Edwin J., additional, Taguchi, Ayumu, additional, and Hanash, Samir M., additional

Published
2017
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28. Abstract 3170: MCAM modulates small cell lung cancer chemoresistance via PI3k/Akt/Sox2 signaling pathway

Author

Tripathi, Satyendra C., primary, Fahrmann, Johannes F., additional, Celiktas, Muge, additional, Aguilar, Mitzi, additional, Marini, Kieren D., additional, Jolly, Mohit K., additional, Katayama, Hiroyuki, additional, Wang, Hong, additional, Murage, Eunice N., additional, Dennison, Jennifer B., additional, Watkins, D. Neil, additional, Levine, Herbert, additional, Ostrin, Edwin J., additional, Taguchi, Ayumu, additional, and Hanash, Samir M., additional

Published
2017
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30. Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Author

Ware, Kathryn E., primary, Gilja, Shivee, primary, Xu, Shenghan, primary, Shetler, Samantha, primary, Jolly, Mohit K., primary, Wang, Xueyang, primary, Bartholf Dewitt, Suzanne, primary, Hish, Alexander J., primary, Jordan, Sarah, primary, Eward, William, primary, Levine, Herbert, primary, Armstrong, Andrew J., primary, and Somarelli, Jason A., primary

Published
2017
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31. Mesenchymal-Epithelial Transition in Sarcomas Is Controlled by the Combinatorial Expression of MicroRNA 200s and GRHL2

Author

Somarelli, Jason A., primary, Shetler, Samantha, additional, Jolly, Mohit K., additional, Wang, Xueyang, additional, Bartholf Dewitt, Suzanne, additional, Hish, Alexander J., additional, Gilja, Shivee, additional, Eward, William C., additional, Ware, Kathryn E., additional, Levine, Herbert, additional, Armstrong, Andrew J., additional, and Garcia-Blanco, Mariano A., additional

Published
2016
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32. Abstract A060: Immunoproteasome deficiency is a feature of NSCLC with a mesenchymal phenotype and is associated with restricted antigen presentation and poor outcome in patients

Author

Tripathi, Satyendra C., primary, Peters, Haley L., additional, Ostrin, Edwin J., additional, Taguchi, Ayumu, additional, Katayama, Hiroyuki, additional, Wang, Hong, additional, Momin, Amin, additional, Jolly, Mohit K., additional, Celiktas, Muge, additional, Rodriguez, Jaime, additional, Behrens, Carmen, additional, Wistuba, Ignacio I., additional, Jacob, Eshel Ben, additional, Levine, Herbert, additional, Molldrem, Jeffrey J., additional, and Hanash, Samir M., additional

Published
2016
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33. Inflammatory breast cancer: A model for investigating cluster-based dissemination

Author

Jolly, Mohit K., Boareto do Amaral, Marcelo, Debeb, Bisrat G., Aceto, Nicola, Farach-Carson, Mary C., Woodward, Wendy A., and Levine, Herbert

Subjects
3. Good health
Abstract

Radiation and chemotherapy are effective treatments for cancer, but are also toxic to healthy cells. Little is known about whether prior exposure to these treatments is related to markers of cellular aging years later in breast cancer survivors. We examined whether past exposure to chemotherapy and/or radiation treatment was associated with DNA damage, telomerase activity, and telomere length 3–6 years after completion of primary treatments in breast cancer survivors (stage 0–IIIA breast cancer at diagnosis). We also examined the relationship of these cellular aging markers with plasma levels of Interleukin (IL)-6, soluble TNF-receptor-II (sTNF-RII), and C-reactive protein (CRP). Ninety-four women (36.4–69.5 years; 80% white) were evaluated. Analyses adjusting for age, race, BMI, and years from last treatment found that women who had prior exposure to chemotherapy and/or radiation compared to women who had previously received surgery alone were more likely to have higher levels of DNA damage (P = .02) and lower telomerase activity (P = .02), but did not have differences in telomere length. More DNA damage and lower telomerase were each associated with higher levels of sTNF-RII (P’s, npj Breast Cancer, 3, ISSN:2374-4677

34. Zinc(II) Complexes of SIRTi1/2 Analogues Transmetallating with Copper Ions and Inducing ROS Mediated Paraptosis.

Author

Kumar A, Chaudhary A, Sonker H, Subhadarshini S, Jolly MK, and Singh RG

Abstract

As the SIRT i analogue series (HL1-HL6) show potent antitumor activity in vitro, we synthesized their corresponding zinc(II) complexes (ZnL1-ZnL6) and investigated their potential as anticancer agents. The Zn(II) complexes showed substantially greater cytotoxicity than HL1-HL6 alone in several cancer cell-types. Notably, distinct structure-activity relationships confirmed the significance of tert -butyl (ZnL2) pharmacophore inclusion in their activity. ZnL2 complexes were found to transmetalate with copper ions inside cells, causing the formation of redox-active copper complexes that induced reactive oxygen species (ROS) production, mitochondrial membrane depolarization, ATP decay, and cell death. This is the first study to exhibit Zn(II) complexes that mediate their activity via transmetalation with copper ions to undergo paraptosis cell death pathway. To further confirm if the SIRT1/2 inhibitory property of SIRTi analogues is conserved, a docking simulation study is performed. The binding affinity and specific interactions of the Cu(II) complex obtained after transmetalation with ZnL2 were found to be higher for SIRT2 ( K i = 0.06 μM) compared to SIRT1 ( K i = 0.25 μM). Thus, the concurrent regulation of several biological targets using a single drug has been shown to have synergistic therapeutic effects, which are crucial for the effective treatment of cancer., Competing Interests: The authors declare no competing financial interest., (© 2024 The Authors. Published by American Chemical Society.)

Published
2024
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