The Expression Regulation and Cancer-Promoting Roles of RACGAP1

RACGAP1 is a Rho-GTPase-activating protein originally discovered in male germ cells to inactivate Rac, RhoA and Cdc42 from the GTP-bound form to the GDP-bound form. GAP has traditionally been known as a tumor suppressor. However, studies increasingly suggest that overexpressed RACGAP1 activates Rac...

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Published inBiomolecules (Basel, Switzerland) Vol. 15; no. 1; p. 3
Main Authors Lin, Jiacheng, Zhu, Yuhao, Lin, Zhaoping, Yu, Jindong, Lin, Xiaobing, Lai, Weiyuan, Tong, Beibei, Xu, Liyan, Li, Enmin, Long, Lin
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 01.01.2025
MDPI
Subjects
Animals
Apoptosis
Bioinformatics
Biomarkers
Breast cancer
Cancer
Cdc42 protein
Cell cycle
Cell division
Cell growth
Colorectal cancer
Cytokinesis
Cytoskeleton
Development and progression
Digestive system
Doxorubicin
ECT2
Gastric cancer
Gene Expression Regulation, Neoplastic
Genetic aspects
Germ cells
GTPase-activating protein
GTPase-Activating Proteins - genetics
GTPase-Activating Proteins - metabolism
Guanine nucleotide-binding protein
Humans
Insects
Kinases
Liver cancer
Mediation
Medical prognosis
Molecules
Neoplasms - genetics
Neoplasms - metabolism
Neoplasms - pathology
Nuclear transport
Oncogenes
Oncology, Experimental
Ovarian cancer
Prostate
Proteins
RACGAP1
Respiratory system
Review
Rho-GTPases
rhoA GTP-Binding Protein - genetics
rhoA GTP-Binding Protein - metabolism
RhoA protein
Signal Transduction
STAT3
Stomach cancer
Therapeutic targets
Tumor suppressor genes
Rho-GTPases
RACGAP1
ECT2
STAT3
Online AccessGet full text

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Abstract RACGAP1 is a Rho-GTPase-activating protein originally discovered in male germ cells to inactivate Rac, RhoA and Cdc42 from the GTP-bound form to the GDP-bound form. GAP has traditionally been known as a tumor suppressor. However, studies increasingly suggest that overexpressed RACGAP1 activates Rac and RhoA in multiple cancers to mediate downstream oncogene overexpression by assisting in the nuclear translocation of signaling molecules and to promote cytokinesis by regulating the cytoskeleton or serving as a component of the central spindle. Contradictorily, it was also reported that RACGAP1 in gastric cancer could inactivate Rac and RhoA. In addition, studies have revealed that RACGAP1 can be a biomarker for prognosis, and its role in reducing doxorubicin sensitivity poses difficulties for treatment, while the current drug targets mainly focus on its downstream molecule. This article mainly reviews the expression regulation of RACGAP1 and its cancer-promoting functions through oncogene expression mediation and Rho-GTPase activation.
AbstractList RACGAP1 is a Rho-GTPase-activating protein originally discovered in male germ cells to inactivate Rac, RhoA and Cdc42 from the GTP-bound form to the GDP-bound form. GAP has traditionally been known as a tumor suppressor. However, studies increasingly suggest that overexpressed RACGAP1 activates Rac and RhoA in multiple cancers to mediate downstream oncogene overexpression by assisting in the nuclear translocation of signaling molecules and to promote cytokinesis by regulating the cytoskeleton or serving as a component of the central spindle. Contradictorily, it was also reported that RACGAP1 in gastric cancer could inactivate Rac and RhoA. In addition, studies have revealed that RACGAP1 can be a biomarker for prognosis, and its role in reducing doxorubicin sensitivity poses difficulties for treatment, while the current drug targets mainly focus on its downstream molecule. This article mainly reviews the expression regulation of RACGAP1 and its cancer-promoting functions through oncogene expression mediation and Rho-GTPase activation.
RACGAP1 is a Rho-GTPase-activating protein originally discovered in male germ cells to inactivate Rac, RhoA and Cdc42 from the GTP-bound form to the GDP-bound form. GAP has traditionally been known as a tumor suppressor. However, studies increasingly suggest that overexpressed RACGAP1 activates Rac and RhoA in multiple cancers to mediate downstream oncogene overexpression by assisting in the nuclear translocation of signaling molecules and to promote cytokinesis by regulating the cytoskeleton or serving as a component of the central spindle. Contradictorily, it was also reported that RACGAP1 in gastric cancer could inactivate Rac and RhoA. In addition, studies have revealed that RACGAP1 can be a biomarker for prognosis, and its role in reducing doxorubicin sensitivity poses difficulties for treatment, while the current drug targets mainly focus on its downstream molecule. This article mainly reviews the expression regulation of RACGAP1 and its cancer-promoting functions through oncogene expression mediation and Rho-GTPase activation.RACGAP1 is a Rho-GTPase-activating protein originally discovered in male germ cells to inactivate Rac, RhoA and Cdc42 from the GTP-bound form to the GDP-bound form. GAP has traditionally been known as a tumor suppressor. However, studies increasingly suggest that overexpressed RACGAP1 activates Rac and RhoA in multiple cancers to mediate downstream oncogene overexpression by assisting in the nuclear translocation of signaling molecules and to promote cytokinesis by regulating the cytoskeleton or serving as a component of the central spindle. Contradictorily, it was also reported that RACGAP1 in gastric cancer could inactivate Rac and RhoA. In addition, studies have revealed that RACGAP1 can be a biomarker for prognosis, and its role in reducing doxorubicin sensitivity poses difficulties for treatment, while the current drug targets mainly focus on its downstream molecule. This article mainly reviews the expression regulation of RACGAP1 and its cancer-promoting functions through oncogene expression mediation and Rho-GTPase activation.
Audience Academic
Author Yu, Jindong
Li, Enmin
Xu, Liyan
Lin, Jiacheng
Lai, Weiyuan
Zhu, Yuhao
Lin, Zhaoping
Tong, Beibei
Long, Lin
Lin, Xiaobing
AuthorAffiliation 3 Institute of Oncologic Pathology, Shantou University Medical College, Shantou 515041, China
1 Department of Biochemistry and Molecular Biology, Shantou University Medical College, Shantou 515041, China
2 The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou 515041, China
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– name: 1 Department of Biochemistry and Molecular Biology, Shantou University Medical College, Shantou 515041, China
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Keywords Rho-GTPases
RACGAP1
ECT2
STAT3
Language English
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Snippet RACGAP1 is a Rho-GTPase-activating protein originally discovered in male germ cells to inactivate Rac, RhoA and Cdc42 from the GTP-bound form to the GDP-bound...
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StartPage 3
SubjectTerms Animals
Apoptosis
Bioinformatics
Biomarkers
Breast cancer
Cancer
Cdc42 protein
Cell cycle
Cell division
Cell growth
Colorectal cancer
Cytokinesis
Cytoskeleton
Development and progression
Digestive system
Doxorubicin
ECT2
Gastric cancer
Gene Expression Regulation, Neoplastic
Genetic aspects
Germ cells
GTPase-activating protein
GTPase-Activating Proteins - genetics
GTPase-Activating Proteins - metabolism
Guanine nucleotide-binding protein
Humans
Insects
Kinases
Liver cancer
Mediation
Medical prognosis
Molecules
Neoplasms - genetics
Neoplasms - metabolism
Neoplasms - pathology
Nuclear transport
Oncogenes
Oncology, Experimental
Ovarian cancer
Prostate
Proteins
RACGAP1
Respiratory system
Review
Rho-GTPases
rhoA GTP-Binding Protein - genetics
rhoA GTP-Binding Protein - metabolism
RhoA protein
Signal Transduction
STAT3
Stomach cancer
Therapeutic targets
Tumor suppressor genes
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Title The Expression Regulation and Cancer-Promoting Roles of RACGAP1
URI https://www.ncbi.nlm.nih.gov/pubmed/39858398
https://www.proquest.com/docview/3159418164
https://www.proquest.com/docview/3159799005
https://pubmed.ncbi.nlm.nih.gov/PMC11760467
https://doaj.org/article/9725121417fd41d8831812e6fb1844b9
Volume 15
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