Ashlin M. Edick

ORCID: 0000-0003-2146-4798
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About
Contact & Profiles
Research Areas
  • DNA Repair Mechanisms
  • RNA modifications and cancer
  • Epigenetics and DNA Methylation
  • CRISPR and Genetic Engineering
  • Polyamine Metabolism and Applications
  • RNA Interference and Gene Delivery
  • Advanced biosensing and bioanalysis techniques
  • DNA and Nucleic Acid Chemistry
  • Animal Genetics and Reproduction
  • PI3K/AKT/mTOR signaling in cancer
  • Metabolism, Diabetes, and Cancer
  • Sirtuins and Resveratrol in Medicine
  • Microtubule and mitosis dynamics
  • RNA Research and Splicing
  • PARP inhibition in cancer therapy
  • Wnt/β-catenin signaling in development and cancer
  • Genomics and Chromatin Dynamics
  • Muscle Physiology and Disorders
  • Hippo pathway signaling and YAP/TAZ

McGill University
2019-2024

University of Guelph
2018-2019

Abstract Colorectal cancer (CRC) is one of the leading causes cancer-related death worldwide. 5-Fluorouracil (5-FU) widely used in treatment cancers, but its antineoplastic activity limited drug-resistant cells. To investigate detailed mechanism 5-FU resistance, we developed a model 5-FU-resistant cells from HCT-8 cells, well-established colorectal cell line. We found that demonstrated high expression TCF4 and β-catenin, indicating an upregulated Wnt pathway. A microarray analysis revealed...

10.1038/s12276-018-0128-8 article EN cc-by Experimental & Molecular Medicine 2018-08-01

Abstract Triple negative breast cancer (TNBC) patients exhibit poor survival outcomes and lack effective targeted therapies. Using unbiased in vivo genome-wide CRISPR screening, we interrogated vulnerabilities TNBC identified an interplay between oncogenic tumor suppressor pathways. This study reveals regulatory functions for essential components of the mTOR Hippo pathways TNBC. vitro drug matrix synergy models patient-derived xenografts, further establish therapeutic relevance our findings...

10.1038/s41467-021-23316-4 article EN cc-by Nature Communications 2021-05-24

Growth factor receptor-bound protein 10 (Grb10) is an adaptor that binds to the insulin receptor, upon which signaling and action are thought be inhibited. Grb10 also a substrate for mechanistic target of rapamycin complex 1 (mTORC1) mediates its feedback inhibition on phosphatidylinositide 3-kinase (PI3K)/Akt signaling. To characterize function regulation by mTORC1 in human muscle, primary skeletal muscle cells were isolated from healthy lean young men then induced differentiate into...

10.1152/ajpendo.00025.2019 article EN AJP Endocrinology and Metabolism 2019-12-03

DNA repair mechanisms are crucial for cell survival. It increases the cancer cell's ability to resist damage. FEN1 is involved in replication and repair, specifically long-patch base excision repair. Although gene function post-translational modification of well studied, regulatory mechanism by upstream signal pathways remains unclear. In this article, we have identified AKT as a regulator activity lung cells. Sustained activation can phosphorylate nuclear transcription factor NF-κB/p65....

10.1158/1535-7163.mct-18-1215 article EN Molecular Cancer Therapeutics 2019-08-29

Multiple DNA repair pathways may be involved in the removal of same lesion caused by endogenous or exogenous agents. Although distinct machinery fulfill overlapping roles lesions, mechanisms coordinating different have not been investigated detail. Here, we show that Ku70, a core protein nonhomologous end‐joining (NHEJ) pathway, can directly interact with polymerase‐β (Pol‐β), central player base excision (BER), and this physical complex only promotes polymerase activity Pol‐β BER efficiency...

10.1096/fj.201900308r article EN The FASEB Journal 2019-07-26

Abstract It has been established that essential amino acids (EAA) regulate protein synthesis in mammary epithelial cells by rapidly altering the phosphorylation state of translation factors. However, long-term transcriptional response to EAA supply investigated much less. Eight transcription factors were selected as candidate mediators effects on cell function via acid ( ATF4 , ATF6 ), mitogen-activated kinase JUN FOS EGR1 and mechanistic target rapamycin complex 1 MYC HIF1A SREBF1 ). The...

10.1101/2024.06.01.596926 preprint EN cc-by bioRxiv (Cold Spring Harbor Laboratory) 2024-06-01

It has been established that essential amino acids (EAA) regulate protein synthesis in mammary epithelial cells by rapidly altering the phosphorylation state of translation factors. However, long-term transcriptional response to EAA supply investigated much less. Eight transcription factors were selected as candidate mediators effects on cell function via acid ( ATF4 , ATF6 ), mitogen-activated kinase JUN FOS EGR1 and mechanistic target rapamycin complex 1 MYC HIF1A SREBF1 ). The objective...

10.1371/journal.pone.0305440 article EN cc-by PLoS ONE 2024-12-20

<div>Abstract<p>DNA repair mechanisms are crucial for cell survival. It increases the cancer cell's ability to resist DNA damage. FEN1 is involved in replication and repair, specifically long-patch base excision repair. Although gene function post-translational modification of well studied, regulatory mechanism by upstream signal pathways remains unclear. In this article, we have identified AKT as a regulator activity lung cells. Sustained activation can phosphorylate nuclear...

10.1158/1535-7163.c.6539584 preprint EN 2023-04-03

<div>Abstract<p>DNA repair mechanisms are crucial for cell survival. It increases the cancer cell's ability to resist DNA damage. FEN1 is involved in replication and repair, specifically long-patch base excision repair. Although gene function post-translational modification of well studied, regulatory mechanism by upstream signal pathways remains unclear. In this article, we have identified AKT as a regulator activity lung cells. Sustained activation can phosphorylate nuclear...

10.1158/1535-7163.c.6539584.v1 preprint EN 2023-04-03
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