Matteo Burigotto
A5074542183- Cancer-related Molecular Pathways
- Cancer Genomics and Diagnostics
- Microtubule and mitosis dynamics
- DNA Repair Mechanisms
- Ubiquitin and proteasome pathways
- Retinal Development and Disorders
- Cancer, Stress, Anesthesia, and Immune Response
- Nanoparticle-Based Drug Delivery
- Pluripotent Stem Cells Research
- CRISPR and Genetic Engineering
- Glioma Diagnosis and Treatment
- Cell death mechanisms and regulation
- Cancer Treatment and Pharmacology
- Autophagy in Disease and Therapy
University of Trento
2020-2023
King's College London
2023
The Francis Crick Institute
2023
Abstract Mutations in the tumor suppressor TP53 cause cancer and impart poor chemotherapeutic responses, reportedly through loss-of-function, dominant-negative effects gain-of-function (GOF) activities. The relative contributions of these attributes is unknown. We found that removal 12 different mutants with reported GOFs by CRISPR/Cas9 did not impact proliferation response to chemotherapeutics 15 human cell lines colon cancer–derived organoids culture. Moreover, mutant TP53/TRP53 impair...
Abstract Centrosome amplification results into genetic instability and predisposes cells to neoplastic transformation. Supernumerary centrosomes trigger p53 stabilization dependent on the PIDDosome (a multiprotein complex composed by PIDD1, RAIDD Caspase‐2), whose activation in cleavage of p53’s key inhibitor, MDM2. Here, we demonstrate that PIDD1 is recruited mature centriolar distal appendage protein ANKRD26. PIDDosome‐dependent Caspase‐2 requires not only centrosomal localization, but...
hTERT-RPE1 cells are genetically stable near diploid widely used to model cell division, DNA repair, or ciliogenesis in a non-transformed context. However, poor transfectability and limited homology-directed repair capacity hamper their amenability gene editing. Here, we describe protocol for rapid efficient generation of diverse homozygous knockins. In contrast other approaches, this strategy bypasses the need molecular cloning. Our approach can also be applied variety types including...
Abstract 53BP1 acts at the crossroads between DNA repair and p53‐mediated stress response. With its interactors p53 USP28, it is part of mitotic surveillance (or stopwatch) pathway (MSP), a sensor that monitors duration cell division, promoting p53‐dependent cycle arrest when critical time threshold surpassed. Here, we show Polo‐like kinase 1 (PLK1) activity essential for time‐dependent release from kinetochores. PLK1 inhibition, which leads to persistence kinetochores, prevents cytosolic...
The PIDDosome is a Caspase-2-activating platform assembling in response to centrosome amplification or genotoxic stress. We have recently shown that both stimuli depend on ANKRD26 (ankyrin repeat domain-containing protein 26)-mediated localization of PIDD1 (p53-inducible with death domain) at the centrosome, demonstrating how this organelle can directly influence cell fate.
<p>Supplementary Figure S24 showing that removal of mutant TP53 does not impair the in vitro growth human colon cancer derived organoids</p>
<p>Supplementary Figure S3 showing that removal of mutant TP53 does not impair the ability diverse human cancer cell lines to adapt conditions stress</p>
<div>Abstract<p>Mutations in the tumor suppressor <i>TP53</i> cause cancer and impart poor chemotherapeutic responses, reportedly through loss-of-function, dominant-negative effects gain-of-function (GOF) activities. The relative contributions of these attributes is unknown. We found that removal 12 different mutants with reported GOFs by CRISPR/Cas9 did not impact proliferation response to chemotherapeutics 15 human cell lines colon cancer–derived organoids culture....
<p>Supplementary Figure S13 showing that mutant TP53 deficient human cancer cell lines retain the machinery to respond activation of wt TP53</p>
<p>Supplementary Figure S11 showing that removal of mutant TP53 does not cause a competitive growth disadvantage in diverse human cancer cell lines culture</p>
<p>Supplementary Figure S14 showing that CRISPR-HDR mediated conversion of mutant TP53 into wt causes a growth disadvantage in human cancer cell lines</p>
<div>Abstract<p>Mutations in the tumor suppressor <i>TP53</i> cause cancer and impart poor chemotherapeutic responses, reportedly through loss-of-function, dominant-negative effects gain-of-function (GOF) activities. The relative contributions of these attributes is unknown. We found that removal 12 different mutants with reported GOFs by CRISPR/Cas9 did not impact proliferation response to chemotherapeutics 15 human cell lines colon cancer–derived organoids culture....
<p>Supplementary Table S6 showing the impact of removal mutant BRAF in human cancer cell lines vitro by CRISPR/Cas9 mining DepMap database</p>
<p>Supplementary Figure S10 showing that complete removal of mutant TP53 in MDA-MB-468 cells does not impair survival and proliferation culture</p>
<p>Supplementary Figure S1 confirming the removal of mutant TP53 in diverse human cancer cell lines</p>
<p>Supplementary Figure S2 showing that removal of mutant TP53 has no impact on survival, proliferation, mitochondrial content and ROS levels in diverse human cancer cell lines</p>
<p>Supplementary Figure S4 showing that removal of mutant TP53 has no impact on survival and proliferation diverse human cancer cell lines when cultured in 3% FCS</p>
<p>Supplementary Figure S1 confirming the removal of mutant TP53 in diverse human cancer cell lines</p>
<p>Supplementary Figure S12 showing that removal of mutant TP53 by RNAi has minor impact on the survival and proliferation certain human cancer cell lines in culture</p>
<p>Supplementary Figure S15 showing that removal of mutant TP53 does not impair in vivo tumor growth certain human cancer cell lines</p>
<p>Supplementary Figure S12 showing that removal of mutant TP53 by RNAi has minor impact on the survival and proliferation certain human cancer cell lines in culture</p>
<p>Supplementary Figure S11 showing that removal of mutant TP53 does not cause a competitive growth disadvantage in diverse human cancer cell lines culture</p>
<p>Supplementary Figure S13 showing that mutant TP53 deficient human cancer cell lines retain the machinery to respond activation of wt TP53</p>
<p>Supplementary Figure S10 showing that complete removal of mutant TP53 in MDA-MB-468 cells does not impair survival and proliferation culture</p>
<p>Supplementary Figure S14 showing that CRISPR-HDR mediated conversion of mutant TP53 into wt causes a growth disadvantage in human cancer cell lines</p>