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Abstract
RhoB, a member of the Ras homolog gene family and GTPase, regulates intracellular signaling pathways by interfacing with epidermal growth factor receptor (EGFR), Ras, and phosphatidylinositol 3-kinase (PI3K)/Akt to modulate responses in cellular structure and function. Notably, the EGFR, Ras, and PI3K/Akt pathways can lead to downregulation of RhoB, while simultaneously being associated with an increased propensity for tumorigenesis. Functionally, RhoB, part of the Rho GTPase family, regulates intracellular signaling pathways by interfacing with EGFR, RAS, and PI3K/Akt/mammalian target of rapamycin (mTOR), and MYC pathways to modulate responses in cellular structure and function. Notably, the EGFR, Ras, and PI3K/Akt pathways can lead to downregulation of RhoB, while simultaneously being associated with an increased propensity for tumorigenesis. RHOB expression has a complex regulatory backdrop consisting of multiple histone deacetyltransferase (HDACs 1 and 6) and microRNA (miR-19a, -21, and -223)-mediated mechanisms of modifying expression. The interwoven nature of RhoB’s regulatory impact and cellular roles in regulating intracellular vesicle trafficking, cell motion, and the cell cycle lays the foundation for analyzing the link between loss of RhoB and tumorigenesis within the context of age-related decline in RhoB. RhoB appears to play a tissue-specific role in tumorigenesis, as such, uncovering and appreciating the potential for restoration of RHOB expression as a mechanism for cancer prevention or therapeutics serves as a practical application. An in-depth assessment of RhoB will serve as a springboard for investigating and characterizing this key component of numerous intracellular messaging and regulatory pathways that may hold the connection between aging and tumorigenesis.
Highlights
Foundational knowledge of the Ras homolog gene family or Rho subgroup of GTPases is critical for further analyzing the multiple interactions that allow for their complicated functions, including regulating cellular actin that modulates cytoskeleton-mediated motion and adhesion, as well as regulating protein trafficking [1,2,3,4,5,6]
It was concluded that resistance to epidermal growth factor receptor (EGFR)-TKI treatment involved the RHOB/Akt signaling and that expression of the RHOB/Akt axis could be utilized as predictor of the response to EGR-TKI
This relationship is made further evident by another study demonstrating that the utilization of pan-Histone Deacetyltransferases (HDACs) inhibitor FK228 leads to upregulation of RHOB expression and promotes growth inhibition of anaplastic thyroid carcinoma cell lines [71]
Summary
Foundational knowledge of the Ras homolog gene family or Rho subgroup of GTPases is critical for further analyzing the multiple interactions that allow for their complicated functions, including regulating cellular actin that modulates cytoskeleton-mediated motion and adhesion, as well as regulating protein trafficking [1,2,3,4,5,6]. Within the Rho subgroup, RhoA, RhoB, and RhoC share significant homology, despite their distinct roles and functional implications in tumorigenesis and aging [10,11]. Protein binding differs between RhoA, RhoB, and RhoC within the hypervariable region, most notably with RhoB harboring a C-terminus that is comprised of significantly more polar amino acid residues, which likely contributes to differential targeting, localization, and rate of ubiquitylation [2,8,19]. Further analysis of RhoB’s unique cellular functions, characterization of its role in tumorigenesis, and exploration of the increasing age with decreasing RHOB expression will shed light on elusive pathways and highlight efforts to expand therapeutic targets
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