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Scattolin, Gloria (2019) Selective killing of T-acute lymphoblastic leukemia (T-ALL) cells by activation of the ROS-OMA1-OPA1 axis. [Ph.D. thesis]

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Abstract (italian or english)

Pediatric T-cell acute lymphoblastic leukemia (T-ALL) is a rare neoplasia accounting for 15% of ALL. Despite significant advances in treatment, approximately one out of five patients develop primary or secondary resistance to current therapies, which include glucocorticoids as a key component; indeed, overall clinical outcome depends on the initial response to glucocorticoids. In our study, we developed an integrated approach to selectively kill T-ALL cells by increasing mitochondrial reactive oxygen species (mtROS). Intracellular ROS are tightly regulated second messengers that affect several signal transduction pathways controlling cell turnover. Oncogenic pathways commonly activated in cancer cells drive a conspicuous increase in production of ROS. Cancer cells commonly exhibit an imbalance between ROS producing pathways and antioxidant defenses that results in a high setpoint of ROS which is close to the threshold beyond which macromolecular damage is produced and cell death pathways are engaged. Therefore, tumor cells are predicted to be more vulnerable than their normal counterparts to treatments that impinge on ROS homeostasis and particularly to agents that blunt antioxidant systems. To increase mtROS levels, we used NS1619, a small molecule that activates the Ca2+-activated K+ (BK) channel, and dehydroepiandrosterone (DHEA), which blunts ROS scavenging through inhibition of the pentose phosphate pathway. These compounds selectively killed T-ALL cell lines, patient-derived xenografts and primary cells from patients (including refractory patients), but did not kill normal human thymocytes. T-ALL cells treated with NS1619 and DHEA showed activation of the ROS-responsive transcription factor NRF2, indicating engagement of antioxidant pathways, as well as increased cleavage of OPA1, a mitochondrial protein that promotes mitochondrial fusion and regulates apoptosis. Consistent with these observations, transmission electron microscopy analysis indicated that NS1619 and DHEA increased mitochondrial fission. OPA1 cleavage and cell death were inhibited by ROS scavengers and by siRNA-mediated knock-down of the mitochondrial protease OMA1, suggesting the engagement of a ROS-OMA1-OPA1 axis in T-ALL cells. Furthermore, NS1619 and DHEA sensitized T-ALL cells to TRAIL-induced apoptosis. Taken together, our findings provide proof-of-principle for an integrated ROS-based pharmacological approach to target refractory T-ALL.

Abstract (a different language)

La leucemia linfoblastica acuta a cellule T (T-ALL) pediatrica è una rara neoplasia che rappresenta all’incirca il 15% delle leucemie linfoblastiche acute. Nonostante i recenti progressi per il trattamento di questa neoplasia, circa un paziente su cinque sviluppa resistenza primaria o secondaria alla terapia, che include i glucocorticoidi come componente principale. In questo progetto abbiamo utilizzato un approccio integrato per uccidere in modo selettivo cellule di T-ALL mediante l’aumento delle specie reattive dell’ossigeno mitocondriali (mtROS). I ROS costituiscono importanti secondi messaggeri che influenzano diverse vie di trasduzione del segnale che regolano la crescita cellulare. Molte vie di segnalazione oncogeniche comunemente iper-attivate nelle cellule tumorali contribuiscono all’aumento dei livelli di ROS, e le cellule tumorali sono spesso caratterizzate da un’aumentata produzione di ROS grazie a un’aumentata difesa antiossidante, che mantiene i livelli di ROS al di sotto dei livelli tossici. Di conseguenza le cellule tumorali dovrebbero essere più sensibili, rispetto a cellule normali, a farmaci che aumentano la produzione di ROS e in particolare a molecole che inibiscono le difese antiossidanti. Per aumentare i livelli di ROS mitocondriali, abbiamo utilizzato l’NS1619, una piccola molecola che attiva il canale del potassio attivato da calcio (BK), e il deidroepiandrosterone (DHEA), il quale, mediante l’inibizione del ciclo dei pentoso fosfati, diminuisce la capacità antiossidante delle cellule. I risultati hanno dimostrato che questi composti sono in grado di uccidere in modo selettivo linee cellulari di T-ALL, patient-derived xenografts e cellule primarie da pazienti in vitro, mentre non inducono morte cellulare di timociti normali. Inoltre, il trattamento di cellule di T-ALL con NS1619 e DHEA induce l’attivazione del fattore di trascrizione indotto da ROS NRF2, indicando il coinvolgimento delle vie antiossidanti. L’aumento di ROS mitocondriali indotto da NS1619 e DHEA induce il clivaggio proteolitico di OPA1, una proteina mitocondriale che promuove la fusione mitocondriale e che regola l’apoptosi. Consistentemente, risultati di microscopia elettronica hanno dimostrato che NS1619 e DHEA aumentano la fissione mitocondriale. I nostri risultati dimostrano inoltre che il taglio proteolitico di OPA1 e la morte cellulare indotta da NS1619 e DHEA sono ridotti da ROS-scavengers e dal silenziamento della proteasi mitocondriale OMA1, suggerendo l’ingaggio dell’asse ROS-OMA1-OPA1. Infine, NS1619 e DHEA sensibilizzano cellule di T-ALL all’apoptosi indotta dal ligando pro-apoptotico TRAIL. In conclusione, i nostri risultati dimostrano che è possibile indurre selettivamente la morte di cellule di T-ALL, indicando nuove possibilità terapeutiche per il trattamento di pazienti refrattari alla terapia.

EPrint type:Ph.D. thesis
Tutor:Ciminale, Vincenzo
Ph.D. course:Ciclo 31 > Corsi 31 > ONCOLOGIA CLINICA E SPERIMENTALE E IMMUNOLOGIA
Data di deposito della tesi:27 November 2018
Anno di Pubblicazione:2019
Key Words:T-ALL, mitochondria, ROS, OMA1. OPA1, TRAIL
Settori scientifico-disciplinari MIUR:Area 06 - Scienze mediche > MED/06 Oncologia medica
Struttura di riferimento:Dipartimenti > Dipartimento di Scienze Chirurgiche Oncologiche e Gastroenterologiche
Codice ID:11398
Depositato il:15 Nov 2019 14:44
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