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Targeting RUNX1 could combat glucocorticoid resistance in patients with lymphoma, according to research published in the Journal of Cellular Biochemistry.
Researchers found an over activity of RUNX1 in lymphoma cells interfered with sphingolipids and caused cells to become resistant to dexamethasone.
Dexamethasone works, in part, through the control of sphingolipid enzymes, which play a role in instructing cells to live or die.
Specifically, the researchers said they found that ectopic expression of RUNX1 in lymphoma cells consistently perturbs the sphingolipid rheostat and confers increased resistance to glucocorticoid-mediated apoptosis.
The team also described the mechanism of cross-talk between glucocorticoid and sphingolipid metabolism through the enzyme Sgpp1.
The researchers said dexamethasone induces expression of Sgpp1 in T-lymphoma cells and drives cell death, which is reduced by partial knockdown of Sgpp1 with short hairpin RNA or direct transcriptional repression of Sgpp1 by ectopic RUNX1.
These findings suggest that drugs targeting RUNX1 may be able to reverse glucocorticoid resistance in lymphoma patients.
“The possibility of making existing therapies more active and specific by combining [them] with drugs that inhibit RUNX is a new and exciting prospect,” said study author James Neil, of The University of Glasgow in Scotland.
“Our collaborators in the US have recently developed drugs that inhibit RUNX, and we plan to test these with existing therapies in blood cancers where MYC and RUNX are both implicated, including multiple myeloma and Burkitt lymphoma.”
An earlier study by Dr Neil and his colleagues suggested that RUNX1 was a potential therapeutic target in MYC-driven lymphomas. 
Image by Ed Uthman
Targeting RUNX1 could combat glucocorticoid resistance in patients with lymphoma, according to research published in the Journal of Cellular Biochemistry.
Researchers found an over activity of RUNX1 in lymphoma cells interfered with sphingolipids and caused cells to become resistant to dexamethasone.
Dexamethasone works, in part, through the control of sphingolipid enzymes, which play a role in instructing cells to live or die.
Specifically, the researchers said they found that ectopic expression of RUNX1 in lymphoma cells consistently perturbs the sphingolipid rheostat and confers increased resistance to glucocorticoid-mediated apoptosis.
The team also described the mechanism of cross-talk between glucocorticoid and sphingolipid metabolism through the enzyme Sgpp1.
The researchers said dexamethasone induces expression of Sgpp1 in T-lymphoma cells and drives cell death, which is reduced by partial knockdown of Sgpp1 with short hairpin RNA or direct transcriptional repression of Sgpp1 by ectopic RUNX1.
These findings suggest that drugs targeting RUNX1 may be able to reverse glucocorticoid resistance in lymphoma patients.
“The possibility of making existing therapies more active and specific by combining [them] with drugs that inhibit RUNX is a new and exciting prospect,” said study author James Neil, of The University of Glasgow in Scotland.
“Our collaborators in the US have recently developed drugs that inhibit RUNX, and we plan to test these with existing therapies in blood cancers where MYC and RUNX are both implicated, including multiple myeloma and Burkitt lymphoma.”
An earlier study by Dr Neil and his colleagues suggested that RUNX1 was a potential therapeutic target in MYC-driven lymphomas.
Image by Ed Uthman
Targeting RUNX1 could combat glucocorticoid resistance in patients with lymphoma, according to research published in the Journal of Cellular Biochemistry.
Researchers found an over activity of RUNX1 in lymphoma cells interfered with sphingolipids and caused cells to become resistant to dexamethasone.
Dexamethasone works, in part, through the control of sphingolipid enzymes, which play a role in instructing cells to live or die.
Specifically, the researchers said they found that ectopic expression of RUNX1 in lymphoma cells consistently perturbs the sphingolipid rheostat and confers increased resistance to glucocorticoid-mediated apoptosis.
The team also described the mechanism of cross-talk between glucocorticoid and sphingolipid metabolism through the enzyme Sgpp1.
The researchers said dexamethasone induces expression of Sgpp1 in T-lymphoma cells and drives cell death, which is reduced by partial knockdown of Sgpp1 with short hairpin RNA or direct transcriptional repression of Sgpp1 by ectopic RUNX1.
These findings suggest that drugs targeting RUNX1 may be able to reverse glucocorticoid resistance in lymphoma patients.
“The possibility of making existing therapies more active and specific by combining [them] with drugs that inhibit RUNX is a new and exciting prospect,” said study author James Neil, of The University of Glasgow in Scotland.
“Our collaborators in the US have recently developed drugs that inhibit RUNX, and we plan to test these with existing therapies in blood cancers where MYC and RUNX are both implicated, including multiple myeloma and Burkitt lymphoma.”
An earlier study by Dr Neil and his colleagues suggested that RUNX1 was a potential therapeutic target in MYC-driven lymphomas.