Forskolin (FSK) induces activation of protein kinase A (PKA). This activation protects specifically some cancer cells from death induced by glucose starvation. Cell effects upon FSK treatment prompted us to investigate in detail the physiological role of PKA in the activation of pro-survival mechanisms in glucose starvation. In this regard we performed a microarray analysis of normal NIH3T3 and transformed NIH3T3-K-ras mouse fibroblasts cultured at 1 mM glucose and daily treated or not with 10 μM FSK until 72 h of growth, when the samples were collected. The microarray is deposited into Gene Expression Omnibus under Series GSE68266. The microarray data revealed that the activation of PKA regulates the expression of genes involved in metabolic, stress-response and pro-survival processes, like glutamine metabolism, autophagy and unfolded protein response, preventing cancer cell death in glucose starvation. Altogether these findings suggest that PKA activation, by inducing a complex transcriptional program, leads to cancer survival in nutrient stress, a typical feature of developing tumor. These transcriptional data, identifying this important role of PKA, will be useful to identify novel target in cancer therapy.

CHIARADONNA, F., PIROLA, Y., RICCIARDIELLO, F., & PALORINI, R. (2016). Transcriptional profiling of immortalized and K-ras-transformed mouse fibroblasts upon PKA stimulation by forskolin in low glucose availability. GENOMICS DATA, 9, 100-104 [10.1016/j.gdata.2016.07.004].

Transcriptional profiling of immortalized and K-ras-transformed mouse fibroblasts upon PKA stimulation by forskolin in low glucose availability

CHIARADONNA, FERDINANDO
Primo
;
PIROLA, YURI
Secondo
;
RICCIARDIELLO, FRANCESCA
Penultimo
;
PALORINI, ROBERTA
Ultimo
2016

Abstract

Forskolin (FSK) induces activation of protein kinase A (PKA). This activation protects specifically some cancer cells from death induced by glucose starvation. Cell effects upon FSK treatment prompted us to investigate in detail the physiological role of PKA in the activation of pro-survival mechanisms in glucose starvation. In this regard we performed a microarray analysis of normal NIH3T3 and transformed NIH3T3-K-ras mouse fibroblasts cultured at 1 mM glucose and daily treated or not with 10 μM FSK until 72 h of growth, when the samples were collected. The microarray is deposited into Gene Expression Omnibus under Series GSE68266. The microarray data revealed that the activation of PKA regulates the expression of genes involved in metabolic, stress-response and pro-survival processes, like glutamine metabolism, autophagy and unfolded protein response, preventing cancer cell death in glucose starvation. Altogether these findings suggest that PKA activation, by inducing a complex transcriptional program, leads to cancer survival in nutrient stress, a typical feature of developing tumor. These transcriptional data, identifying this important role of PKA, will be useful to identify novel target in cancer therapy.
Articolo in rivista - Articolo scientifico
Cancer cell resistance; Cancer metabolism; Glucose starvation; Protein kinase A (PKA);
Cancer cell resistance; Cancer metabolism; Glucose starvation; Protein kinase A (PKA); Biotechnology; Biochemistry; Molecular Medicine; Genetics
English
100
104
5
CHIARADONNA, F., PIROLA, Y., RICCIARDIELLO, F., & PALORINI, R. (2016). Transcriptional profiling of immortalized and K-ras-transformed mouse fibroblasts upon PKA stimulation by forskolin in low glucose availability. GENOMICS DATA, 9, 100-104 [10.1016/j.gdata.2016.07.004].
Chiaradonna, F; Pirola, Y; Ricciardiello, F; Palorini, R
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/135109
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