Mara Cirone | Ricerc@Sapienza

Pubblicazioni

Titolo	Pubblicato in	Anno
P62/sqstm1/keap1/nrf2 axis reduces cancer cells death-sensitivity in response to zn(Ii)–curcumin complex	BIOMOLECULES	2021
The cross-talk between STAT1/STAT3 and ROS up-regulates PD-L1 and promotes the release of pro-inflammatory/immune suppressive cytokines in primary monocytes infected by HHV-6B	VIRUS RESEARCH	2021
PGE2 released by pancreatic cancer cells undergoing ER stress transfers the stress to DCs impairing their immune function	MOLECULAR CANCER THERAPEUTICS	2021
Oncogenic pathways activated by pro-inflammatory cytokines promote mutant p53 stability: clue for novel anticancer therapies	CELLULAR AND MOLECULAR LIFE SCIENCES	2021
Er stress, upr activation and the inflammatory response to viral infection	VIRUSES	2021
Antiviral filtering capacity of go-coated textiles	APPLIED SCIENCES	2021
Role of upr sensor activation in cell death–survival decision of colon cancer cells stressed by dpe treatment	BIOMEDICINES	2021
Anticancer effect of AZD2461 PARP inhibitor against colon cancer cells carrying wt or dysfunctional p53	EXPERIMENTAL CELL RESEARCH	2021
New insights into curcumin-and resveratrol-mediated anti-cancer effects	PHARMACEUTICALS	2021
Cancer cells dysregulate PI3K/AKT/mTOR pathway activation to ensure their survival and proliferation: mimicking them is a smart strategy of gammaherpesviruses	CRITICAL REVIEWS IN BIOCHEMISTRY AND MOLECULAR BIOLOGY	2021
Lovastatin reduces PEL cell survival by phosphorylating ERK1/2 that blocks the autophagic flux and engages a cross-talk with p53 to activate p21	IUBMB LIFE	2021
HHV-6A infection dysregulates autophagy/UPR interplay increasing beta amyloid production and tau phosphorylation in astrocytoma cells as well as in primary neurons, possible molecular mechanisms linking viral infection to Alzheimer's disease	BIOCHIMICA ET BIOPHYSICA ACTA. MOLECULAR BASIS OF DISEASE	2020
Interplay between endoplasmic reticulum (ER) stress and autophagy induces mutant p53H273 degradation	BIOMOLECULES	2020
PBA preferentially impairs cell survival of glioblastomas carrying mutp53 by reducing its expression level, stabilizing wtp53, downregulating the mevalonate kinase and dysregulating UPR	BIOMOLECULES	2020
KSHV infection skews macrophage polarisation towards M2-like/TAM and activates Ire1 α-XBP1 axis up-regulating pro-tumorigenic cytokine release and PD-L1 expression	BRITISH JOURNAL OF CANCER	2020
Perturbation of bulk and selective macroautophagy, abnormal UPR activation and their interplay pave the way to immune dysfunction, cancerogenesis and neurodegeneration in ageing	AGEING RESEARCH REVIEWS	2020
A ruthenium(II)-curcumin compound modulates NRF2 expression balancing the cancer cell death/survival outcome according to p53 status	JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH	2020
KSHV dysregulates bulk macroautophagy, mitophagy and UPR to promote endothelial to mesenchymal transition and CCL2 release, key events in viral-driven sarcomagenesis	INTERNATIONAL JOURNAL OF CANCER	2020
BFRF1 protein is involved in EBV-mediated autophagy manipulation	MICROBES AND INFECTION	2020
STAT3 and mutp53 Engage a Positive Feedback Loop Involving HSP90 and the Mevalonate Pathway	FRONTIERS IN ONCOLOGY	2020

ERC

LS1_2
LS1_9
LS4_12
LS6
LS6_5

Interessi di ricerca

Oncoimmunologia Virale. Autofagia nella cancerogenesi virale e chimica. Target therapies e UPR e autophagy targeting nel cancro.

Keywords

Herpesvirus 4

BASI BIOLOGICHE DEL CANCRO

anti-tumor immune response

Herpesvirus 8

endoplasmic reticulum (ER stress)

Progetti di Ricerca

Exploitng the interplay between Unfolded Protein Response and DNA damage response to potentiate the efficacy of anticancer therapies
Manipulation of UPR and PRR signaling as strategy to reduce the side effects of herpesvirus-induced inflammation.
Coinvolgimento dell'autofagia nella trasformazione maligna mediata da EBV e KSHV.
Manipolazione dell'autofagia e dell'effetto Warbourg come strategia per modificare il cross-talk tra cellule tumorali KSHV-associate e microambiente tumorale
Manipulation of UPR in tumor cells and dendritic cells or macrophages exposed to tumor released factors to counteract tumor-induced immune dysfunction .