Ask about this productRelated genes to: RAB22A antibody
- Gene:
- RAB22A NIH gene
- Name:
- RAB22A, member RAS oncogene family
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 20q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-31
- Date modifiied:
- 2016-10-05
Related products to: RAB22A antibody
Related articles to: RAB22A antibody
- N6-methyladenosine (mA) modification has emerged as a critical post-transcriptional regulatory mechanism in osteoarthritis (OA). However, the contribution of mA-dependent regulation of circular RNAs (circRNAs) to chondrocyte senescence and OA progression remains poorly understood. We aimed to elucidate whether mA-mediated control of circRNAs regulates chondrocyte senescence and to define the underlying molecular mechanisms contributing to OA progression. Here, we identified an OA-associated circRNA, circHIPK2, and demonstrated that its abundance and function are regulated by an mA reader-dependent decay mechanism. circHIPK2 expression was reduced in human OA cartilage, and its depletion exacerbated chondrocyte senescence, increased senescence-associated secretory phenotype (SASP) gene expression, and impaired autophagy both in vitro and in the destabilization of the medial meniscus (DMM) model. Mechanistically, YTH N-methyladenosine RNA-binding protein 2 (YTHDF2) recognized mA-modified circHIPK2 and facilitated its degradation, thereby reducing circHIPK2 stability. Functionally, circHIPK2 directly interacted with RAB22A. Loss of circHIPK2 weakened this interaction, enhanced RAB22A-PI3K association, activated the PI3K-AKT-mTOR signaling pathway, disrupted autophagic flux, and accelerated senescence-associated phenotypes. Notably, the protective effects of circHIPK2 were abolished in RAB22A-binding-deficient circHIPK2 mutants, establishing a direct link between molecular interaction and functional outcome. Furthermore, we encapsulated circHIPK2 into lipid nanoparticles (circHIPK2-LNP) for transient intra-articular delivery. Intra-articular administration of circHIPK2-LNP attenuated chondrocyte senescence and alleviated OA progression in DMM mice. Collectively, mA-dependent YTHDF2-mediated degradation of circHIPK2 promotes chondrocyte senescence and OA progression by disrupting autophagy, identifying circHIPK2 as a potential therapeutic target and prognostic biomarker for cartilage aging in OA. - Source: PubMed
Publication date: 2026/03/27
Long DianboLin ZhencanLi ZhiwenLi MingZhao XiaoyiDeng ZengfaJiang ZongruiLi WeiZhong YanlinHe AishanXu YiyangMao GupingKang Yan - Chemoresistance is not only related to tumor cells themselves, but also regulated by the interaction between cells in the tumor microenvironment (TME). However, the underlying mechanisms are not well understood. RAB22A, a member of the RAB family of small GTPases that was identified by our group previously as an oncogene in colorectal cancer (CRC). In this study, we demonstrated that elevated expression of RAB22A in CRC cells, particularly in chemoresistant CRC cells, is associated with increased exosome secretion and enhanced chemoresistance. Mechanistically, RAB22A augments exosome secretion by inhibiting the ubiquitination and degradation of pyruvate kinase type M2 (PKM2), then promoting the phosphorylation of synaptosome-associated protein 23 (SNAP-23). Furthermore, RAB22A not only directly promotes chemoresistance in CRC cells but also indirectly induces acquired drug resistance of other CRC cells in the TME by promoting the secretion of RAB22A-PKM2-rich exosomes, thereby triggering intercellular chemoresistance transmission. Together, we reveal an essential role of RAB22A-PKM2-SNAP-23 signaling cascade in exosome induction in chemoresistant CRC cells and intercellular chemoresistance transmission, highlighting that targeting the RAB22A/PKM2/pSNAP axis is a potential novel strategy to reverse chemoresistance, and suggest circulating exosomal RAB22A and PKM2 as markers to predict the efficacy of chemotherapy in CRC. - Source: PubMed
Publication date: 2025/09/16
Yin YuanMing LiangQin YanTang JunhuiLiu BingxinLiu YuhangJin GuoyingJiang LingzhenYao SuruiQi XiaoweiHuang Zhaohui - Colorectal cancer metastasis remains a major cause of cancer-related mortality, with the Metastasis-Associated in Colon Cancer 1 (MACC1) protein emerging as a critical regulator of tumor progression. Although exosomes are recognized mediators of oncogenic communication, the interplay between MACC1 and exosome biology is yet to be fully explored. This study unveils a dual mechanism through which MACC1 coordinates exosome biogenesis and oncogenic cargo delivery to drive metastatic progression. We first established clinical relevance by Pearson's demonstrating a significant correlation between MACC1 expression and exosome concentration in colorectal tumors (r = 0.457, P < 0.05). Functional studies showed that MACC1-overexpressing HCT116 cells exhibited enhanced invasiveness and transmitted pro-metastatic signals via exosomes. These exosomes were significantly enriched in the c-Met oncoprotein (P < 0.05 vs. controls) and could induce epithelial-mesenchymal transition in recipient SW480 cells, significantly enhancing their migration and invasion capacities. Mechanistically, transcriptomic analysis identified several components of the exosome secretion machinery (YKT6, RAB22A, and VPS41) as downstream targets of MACC1. Promoter-binding assays confirmed that MACC1 directly activates the transcription of YKT6, a member of the Soluble N-ethylmaleimide-sensitive factor attachment protein receptor family. This protein is critical for multivesicular body-plasma membrane fusion. The transcriptional activation led to cytoplasmic accumulation of YKT6 (P < 0.05), driving a 2.9-fold increase in exosome secretion. Crucially, YKT6-mediated exosome hypersecretion facilitated the extracellular release of c-Met-enriched vesicles, establishing a feed-forward loop for metastatic propagation. Our findings delineate an integrated metastatic axis: MACC1 orchestrates (1) transcriptional upregulation of YKT6 to amplify exosome production, and (2) selective packaging of c-Met into exosomes that prime recipient cells for invasion. This dual regulatory mechanism highlights potential therapeutic targets for intercepting metastasis-specific exosome signaling in colorectal cancer. - Source: PubMed
Publication date: 2025/08/18
Hou ShenghuaiWang LingxiaoYang ChongLi YaopingLiu Haiyi - Gastric cancer (GC) is a highly prevalent and lethal malignancy worldwide. Accumulating evidence has shown that microRNAs (miRNAs) play essential roles in the development and progression of GC. In this study, we aimed to investigate the expression, functions, and molecular mechanisms of miRNA-204-5p in GC. We found that miRNA-204-5p was significantly downregulated in GC cell lines compared to their normal counterparts. Functional experiments demonstrated that miRNA-204-5p inhibited the migration, invasion, and glycolysis of GC cells in vitro and suppressed tumor lung metastasis in vivo. Mechanistically, miRNA-204-5p exerted its tumor-suppressive effects by directly targeting RAB22A and inhibiting the PI3K/AKT signaling pathway. Overexpression of RAB22A partially reversed the inhibitory effects of miRNA-204-5p on the malignant phenotypes and the PI3K/AKT pathway activation in GC cells. Furthermore, miRNA-204-5p regulated the expression of molecules related to epithelial-mesenchymal transition, and glycolysis through the RAB22A/PI3K/AKT axis. Our findings suggest that miRNA-204-5p functions as a tumor suppressor in GC by targeting RAB22A and provide novel insights into the molecular mechanisms underlying GC progression. The miRNA-204-5p/RAB22A axis may serve as a potential diagnostic biomarker and therapeutic target for GC. - Source: PubMed
Publication date: 2025/08/12
Pan WenTan YingChen XiaohongZeng LiLv YuetongYang Jinlin - Regenerative processes occur at various levels in all organisms, yet their complexity continues to raise new questions about their mechanisms. It has been demonstrated that small extracellular vesicles (sEVs), secreted by all cells and influencing their function, play a significant role in regeneration. In the context of regenerative processes, oral mucosal tissues consistently receive interest, as they are among the most rapidly healing tissues in the human body. In this study, we utilized spatial transcriptomics to map gene expression to specific spatial locations within the gingiva tissue section, using publicly available transcriptomic data. This analysis revealed new insights into this tissue and the biogenesis of sEVs within it. The identified clusters encompassed two main regions-the epithelium and lamina propria-as well as minor niches within them. Using Gene Ontology (GO) analysis, we identified two clusters most enriched in extracellular vesicle-related GO processes. These included the superficial and deeper layers of the sulcular epithelium, one of the most peripheral regions of the gingiva. Of the 43 genes identified in the literature as having a potential or documented role in sEVs biogenesis, 12 were selected for further analysis. , , and showed clear specificity and the highest expression in the superficial layer of the sulcular epithelium. also exhibited high expression in this layer, though its levels were comparable to the outer layer of the oral epithelium. Other well-established sEVs marker genes, such as , , , , , , , and , were also expressed in the examined tissue; however, their expression was not specifically exclusive to the sulcular epithelium. Our study is the first to perform a meta-analysis of available gingival transcriptomic data in the specific context of sEVs biogenesis. The presented data and conclusions provide new insights into the role of different structures within healthy human gingiva and shed new light on both known and potential markers of sEVs biogenesis. These findings may contribute to the development of regeneration-targeted research, especially on oral tissues. - Source: PubMed
Publication date: 2025/04/07
Borowiec Blanka MariaBlatkiewicz MałgorzataDyszkiewicz-Konwińska MartaBukowska DorotaKempisty BartoszRuciński MarcinNowicki MichałBudna-Tukan Joanna