RALB GTPase: a critical regulator of DR5 expression and TRAIL sensitivity in KRAS mutant colorectal cancer
RAS mutant (MT) metastatic colorectal cancer (mCRC) is resistant to MEK1/2 inhibition and remains a difficult-to-treat group. Therefore, there is an unmet need for novel treatment options for RAS MT mCRC. RALA and RALB GTPases function downstream of RAS and have been found to be key regulators of se...
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| Vydáno v: | Cell death & disease Ročník 11; číslo 10; s. 930 |
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| Hlavní autoři: | , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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Nature Publishing Group UK
29.10.2020
Springer Nature B.V Nature Publishing Group |
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| ISSN: | 2041-4889, 2041-4889 |
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| Abstract | RAS
mutant (MT) metastatic colorectal cancer (mCRC) is resistant to MEK1/2 inhibition and remains a difficult-to-treat group. Therefore, there is an unmet need for novel treatment options for
RAS
MT mCRC. RALA and RALB GTPases function downstream of RAS and have been found to be key regulators of several cell functions implicated in KRAS-driven tumorigenesis. However, their role as regulators of the apoptotic machinery remains to be elucidated. Here, we found that inhibition of RALB expression, but not RALA, resulted in Caspase-8-dependent cell death in
KRAS
MT CRC cells, which was not further increased following MEK1/2 inhibition. Proteomic analysis and mechanistic studies revealed that RALB depletion induced a marked upregulation of the pro-apoptotic cell surface TRAIL Death Receptor 5 (DR5) (also known as TRAIL-R2), primarily through modulating DR5 protein lysosomal degradation. Moreover, DR5 knockdown or knockout attenuated siRALB-induced apoptosis, confirming the role of the extrinsic apoptotic pathway as a regulator of siRALB-induced cell death. Importantly, TRAIL treatment resulted in the association of RALB with the death-inducing signalling complex (DISC) and targeting RALB using pharmacologic inhibition or RNAi approaches triggered a potent increase in TRAIL-induced cell death in
KRAS
MT CRC cells. Significantly, high
RALB
mRNA levels were found in the poor prognostic Colorectal Cancer Intrinsic Subtypes (CRIS)-B CRC subgroup. Collectively, this study provides to our knowledge the first evidence for a role for RALB in apoptotic priming and suggests that RALB inhibition may be a promising strategy to improve response to TRAIL treatment in poor prognostic
RAS
MT CRIS-B CRC. |
|---|---|
| AbstractList | RAS
mutant (MT) metastatic colorectal cancer (mCRC) is resistant to MEK1/2 inhibition and remains a difficult-to-treat group. Therefore, there is an unmet need for novel treatment options for
RAS
MT mCRC. RALA and RALB GTPases function downstream of RAS and have been found to be key regulators of several cell functions implicated in KRAS-driven tumorigenesis. However, their role as regulators of the apoptotic machinery remains to be elucidated. Here, we found that inhibition of RALB expression, but not RALA, resulted in Caspase-8-dependent cell death in
KRAS
MT CRC cells, which was not further increased following MEK1/2 inhibition. Proteomic analysis and mechanistic studies revealed that RALB depletion induced a marked upregulation of the pro-apoptotic cell surface TRAIL Death Receptor 5 (DR5) (also known as TRAIL-R2), primarily through modulating DR5 protein lysosomal degradation. Moreover, DR5 knockdown or knockout attenuated siRALB-induced apoptosis, confirming the role of the extrinsic apoptotic pathway as a regulator of siRALB-induced cell death. Importantly, TRAIL treatment resulted in the association of RALB with the death-inducing signalling complex (DISC) and targeting RALB using pharmacologic inhibition or RNAi approaches triggered a potent increase in TRAIL-induced cell death in
KRAS
MT CRC cells. Significantly, high
RALB
mRNA levels were found in the poor prognostic Colorectal Cancer Intrinsic Subtypes (CRIS)-B CRC subgroup. Collectively, this study provides to our knowledge the first evidence for a role for RALB in apoptotic priming and suggests that RALB inhibition may be a promising strategy to improve response to TRAIL treatment in poor prognostic
RAS
MT CRIS-B CRC. RAS mutant (MT) metastatic colorectal cancer (mCRC) is resistant to MEK1/2 inhibition and remains a difficult-to-treat group. Therefore, there is an unmet need for novel treatment options for RASMT mCRC. RALA and RALB GTPases function downstream of RAS and have been found to be key regulators of several cell functions implicated in KRAS-driven tumorigenesis. However, their role as regulators of the apoptotic machinery remains to be elucidated. Here, we found that inhibition of RALB expression, but not RALA, resulted in Caspase-8-dependent cell death in KRASMT CRC cells, which was not further increased following MEK1/2 inhibition. Proteomic analysis and mechanistic studies revealed that RALB depletion induced a marked upregulation of the pro-apoptotic cell surface TRAIL Death Receptor 5 (DR5) (also known as TRAIL-R2), primarily through modulating DR5 protein lysosomal degradation. Moreover, DR5 knockdown or knockout attenuated siRALB-induced apoptosis, confirming the role of the extrinsic apoptotic pathway as a regulator of siRALB-induced cell death. Importantly, TRAIL treatment resulted in the association of RALB with the death-inducing signalling complex (DISC) and targeting RALB using pharmacologic inhibition or RNAi approaches triggered a potent increase in TRAIL-induced cell death in KRASMT CRC cells. Significantly, high RALB mRNA levels were found in the poor prognostic Colorectal Cancer Intrinsic Subtypes (CRIS)-B CRC subgroup. Collectively, this study provides to our knowledge the first evidence for a role for RALB in apoptotic priming and suggests that RALB inhibition may be a promising strategy to improve response to TRAIL treatment in poor prognostic RASMT CRIS-B CRC.RAS mutant (MT) metastatic colorectal cancer (mCRC) is resistant to MEK1/2 inhibition and remains a difficult-to-treat group. Therefore, there is an unmet need for novel treatment options for RASMT mCRC. RALA and RALB GTPases function downstream of RAS and have been found to be key regulators of several cell functions implicated in KRAS-driven tumorigenesis. However, their role as regulators of the apoptotic machinery remains to be elucidated. Here, we found that inhibition of RALB expression, but not RALA, resulted in Caspase-8-dependent cell death in KRASMT CRC cells, which was not further increased following MEK1/2 inhibition. Proteomic analysis and mechanistic studies revealed that RALB depletion induced a marked upregulation of the pro-apoptotic cell surface TRAIL Death Receptor 5 (DR5) (also known as TRAIL-R2), primarily through modulating DR5 protein lysosomal degradation. Moreover, DR5 knockdown or knockout attenuated siRALB-induced apoptosis, confirming the role of the extrinsic apoptotic pathway as a regulator of siRALB-induced cell death. Importantly, TRAIL treatment resulted in the association of RALB with the death-inducing signalling complex (DISC) and targeting RALB using pharmacologic inhibition or RNAi approaches triggered a potent increase in TRAIL-induced cell death in KRASMT CRC cells. Significantly, high RALB mRNA levels were found in the poor prognostic Colorectal Cancer Intrinsic Subtypes (CRIS)-B CRC subgroup. Collectively, this study provides to our knowledge the first evidence for a role for RALB in apoptotic priming and suggests that RALB inhibition may be a promising strategy to improve response to TRAIL treatment in poor prognostic RASMT CRIS-B CRC. RAS mutant (MT) metastatic colorectal cancer (mCRC) is resistant to MEK1/2 inhibition and remains a difficult-to-treat group. Therefore, there is an unmet need for novel treatment options for RASMT mCRC. RALA and RALB GTPases function downstream of RAS and have been found to be key regulators of several cell functions implicated in KRAS-driven tumorigenesis. However, their role as regulators of the apoptotic machinery remains to be elucidated. Here, we found that inhibition of RALB expression, but not RALA, resulted in Caspase-8-dependent cell death in KRASMT CRC cells, which was not further increased following MEK1/2 inhibition. Proteomic analysis and mechanistic studies revealed that RALB depletion induced a marked upregulation of the pro-apoptotic cell surface TRAIL Death Receptor 5 (DR5) (also known as TRAIL-R2), primarily through modulating DR5 protein lysosomal degradation. Moreover, DR5 knockdown or knockout attenuated siRALB-induced apoptosis, confirming the role of the extrinsic apoptotic pathway as a regulator of siRALB-induced cell death. Importantly, TRAIL treatment resulted in the association of RALB with the death-inducing signalling complex (DISC) and targeting RALB using pharmacologic inhibition or RNAi approaches triggered a potent increase in TRAIL-induced cell death in KRASMT CRC cells. Significantly, high RALB mRNA levels were found in the poor prognostic Colorectal Cancer Intrinsic Subtypes (CRIS)-B CRC subgroup. Collectively, this study provides to our knowledge the first evidence for a role for RALB in apoptotic priming and suggests that RALB inhibition may be a promising strategy to improve response to TRAIL treatment in poor prognostic RASMT CRIS-B CRC. |
| ArticleNumber | 930 |
| Author | Van Schaeybroeck, Sandra Kennedy, Richard Harrison, Timothy Scott, Christopher J. McArt, Darragh Longley, Daniel B. Campbell, Andrew Rehm, Markus Di Nicolantonio, Federica O’Reilly, Paul Bardelli, Alberto Majkut, Joanna Sansom, Owen J. Allen, Wendy L. Roberts, Jamie Z. Javadi, Arman Vitale, Nicolas Khawaja, Hajrah Evergren, Emma |
| Author_xml | – sequence: 1 givenname: Hajrah orcidid: 0000-0001-6015-259X surname: Khawaja fullname: Khawaja, Hajrah organization: Drug Resistance Group, Patrick G. Johnston Centre for Cancer Research, School of Medicine, Dentistry and Biomedical Science, Queen’s University Belfast – sequence: 2 givenname: Andrew surname: Campbell fullname: Campbell, Andrew organization: Cancer Research UK Beatson Institute – sequence: 3 givenname: Jamie Z. surname: Roberts fullname: Roberts, Jamie Z. organization: Drug Resistance Group, Patrick G. Johnston Centre for Cancer Research, School of Medicine, Dentistry and Biomedical Science, Queen’s University Belfast – sequence: 4 givenname: Arman surname: Javadi fullname: Javadi, Arman organization: Drug Resistance Group, Patrick G. Johnston Centre for Cancer Research, School of Medicine, Dentistry and Biomedical Science, Queen’s University Belfast – sequence: 5 givenname: Paul surname: O’Reilly fullname: O’Reilly, Paul organization: Drug Resistance Group, Patrick G. Johnston Centre for Cancer Research, School of Medicine, Dentistry and Biomedical Science, Queen’s University Belfast – sequence: 6 givenname: Darragh surname: McArt fullname: McArt, Darragh organization: Drug Resistance Group, Patrick G. Johnston Centre for Cancer Research, School of Medicine, Dentistry and Biomedical Science, Queen’s University Belfast – sequence: 7 givenname: Wendy L. surname: Allen fullname: Allen, Wendy L. organization: Drug Resistance Group, Patrick G. Johnston Centre for Cancer Research, School of Medicine, Dentistry and Biomedical Science, Queen’s University Belfast – sequence: 8 givenname: Joanna surname: Majkut fullname: Majkut, Joanna organization: Drug Resistance Group, Patrick G. Johnston Centre for Cancer Research, School of Medicine, Dentistry and Biomedical Science, Queen’s University Belfast – sequence: 9 givenname: Markus orcidid: 0000-0001-6149-9261 surname: Rehm fullname: Rehm, Markus organization: Institute of Cell Biology and Immunology, University of Stuttgart – sequence: 10 givenname: Alberto surname: Bardelli fullname: Bardelli, Alberto organization: Department of Oncology, University of Torino, Candiolo Cancer Institute, FPO-IRCCS – sequence: 11 givenname: Federica orcidid: 0000-0001-9618-2010 surname: Di Nicolantonio fullname: Di Nicolantonio, Federica organization: Department of Oncology, University of Torino, Candiolo Cancer Institute, FPO-IRCCS – sequence: 12 givenname: Christopher J. surname: Scott fullname: Scott, Christopher J. organization: Drug Resistance Group, Patrick G. Johnston Centre for Cancer Research, School of Medicine, Dentistry and Biomedical Science, Queen’s University Belfast – sequence: 13 givenname: Richard surname: Kennedy fullname: Kennedy, Richard organization: Drug Resistance Group, Patrick G. Johnston Centre for Cancer Research, School of Medicine, Dentistry and Biomedical Science, Queen’s University Belfast – sequence: 14 givenname: Nicolas surname: Vitale fullname: Vitale, Nicolas organization: Centre National de la Recherche Scientifique, Université de Strasbourg, Institut des Neurosciences Cellulaires et Intégratives – sequence: 15 givenname: Timothy surname: Harrison fullname: Harrison, Timothy organization: Drug Resistance Group, Patrick G. Johnston Centre for Cancer Research, School of Medicine, Dentistry and Biomedical Science, Queen’s University Belfast – sequence: 16 givenname: Owen J. orcidid: 0000-0001-9540-3010 surname: Sansom fullname: Sansom, Owen J. organization: Cancer Research UK Beatson Institute, Institute of Cancer Sciences, University of Glasgow – sequence: 17 givenname: Daniel B. surname: Longley fullname: Longley, Daniel B. organization: Drug Resistance Group, Patrick G. Johnston Centre for Cancer Research, School of Medicine, Dentistry and Biomedical Science, Queen’s University Belfast – sequence: 18 givenname: Emma surname: Evergren fullname: Evergren, Emma organization: Drug Resistance Group, Patrick G. Johnston Centre for Cancer Research, School of Medicine, Dentistry and Biomedical Science, Queen’s University Belfast – sequence: 19 givenname: Sandra surname: Van Schaeybroeck fullname: Van Schaeybroeck, Sandra email: s.vanschaeybroeck@qub.ac.uk organization: Drug Resistance Group, Patrick G. Johnston Centre for Cancer Research, School of Medicine, Dentistry and Biomedical Science, Queen’s University Belfast |
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| CitedBy_id | crossref_primary_10_1016_j_humpath_2023_09_011 crossref_primary_10_1002_cam4_71202 crossref_primary_10_3389_fgene_2021_690530 crossref_primary_10_3390_cells11101645 crossref_primary_10_3390_cancers13133351 crossref_primary_10_1007_s42764_022_00059_0 crossref_primary_10_1158_1541_7786_MCR_24_0151 crossref_primary_10_3390_cancers13153757 crossref_primary_10_1186_s12943_025_02358_y crossref_primary_10_3390_molecules26247582 |
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| SSID | ssj0000330256 |
| Score | 2.338407 |
| Snippet | RAS
mutant (MT) metastatic colorectal cancer (mCRC) is resistant to MEK1/2 inhibition and remains a difficult-to-treat group. Therefore, there is an unmet need... RAS mutant (MT) metastatic colorectal cancer (mCRC) is resistant to MEK1/2 inhibition and remains a difficult-to-treat group. Therefore, there is an unmet need... |
| SourceID | pubmedcentral hal proquest pubmed crossref springer |
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| SubjectTerms | 13/2 13/31 13/89 14/19 38/109 38/79 42/70 631/67/1504/1885/1393 631/67/395 631/80/82/23 82/80 96/106 96/95 Antibodies Antineoplastic Combined Chemotherapy Protocols - pharmacology Apoptosis Benzimidazoles - administration & dosage Biochemistry Biomedical and Life Sciences Cancer Caspase-8 Cell Biology Cell Culture Cell death Cell surface Cellular Biology Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - drug therapy Colorectal Neoplasms - genetics Colorectal Neoplasms - metabolism DR5 protein GTP Phosphohydrolases - metabolism Humans Immunology K-Ras protein Life Sciences Lysosomes Metastases mRNA Mutants Mutation Proto-Oncogene Proteins p21(ras) - genetics Proto-Oncogene Proteins p21(ras) - metabolism ral GTP-Binding Proteins - antagonists & inhibitors ral GTP-Binding Proteins - biosynthesis ral GTP-Binding Proteins - genetics ral GTP-Binding Proteins - metabolism RalA protein Ras protein Receptors, TNF-Related Apoptosis-Inducing Ligand - agonists Receptors, TNF-Related Apoptosis-Inducing Ligand - metabolism Recombinant Proteins - pharmacology RNA, Messenger - genetics RNA, Messenger - metabolism RNA-mediated interference Signal transduction TNF-Related Apoptosis-Inducing Ligand - administration & dosage TNF-Related Apoptosis-Inducing Ligand - pharmacology Transfection Tumorigenesis |
| Title | RALB GTPase: a critical regulator of DR5 expression and TRAIL sensitivity in KRAS mutant colorectal cancer |
| URI | https://link.springer.com/article/10.1038/s41419-020-03131-3 https://www.ncbi.nlm.nih.gov/pubmed/33122623 https://www.proquest.com/docview/2471532479 https://www.proquest.com/docview/2456413142 https://hal.science/hal-03360660 https://pubmed.ncbi.nlm.nih.gov/PMC7596570 |
| Volume | 11 |
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