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Insights into the complex interactions between Rab22a and extracellular vesicles in cancers

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Abstract

Introduction

Oncogenic Ras-related GTP-binding proteins, referred to as Rabs, are characterized by their intricate interactions with upstream, downstream molecules, and notably, extracellular vesicles (EVs). While the expansive family of Rabs and their associated signaling pathways have been exhaustively dissected, Rab22a emerges as an entity of outstanding interest, owing to its potent influence in many biological processes and its conspicuous correlation with cancer metastasis and migration. A burgeoning interest in the interactions between Rab22a and EVs in the field of oncology underscores the necessity for more in-depth reviews and scholarly discourses.

Methods

We performed a review based on published original and review articles related to Rab22a, tumor, microRNA, exosome, microvesicles, EVs, CD147, lysosome, degradation, endosomal recycling, etc. from PubMed, Web of Science and Google Scholar databases.

Results and conclusions

We summarize the regulatory processes governing the expression of Rab22a and the mutants of Rab22a. Notably, the present understanding of complex interactions between Rab22a and EVs are highlighted, encompassing both the impact of Rab22a on the genesis of EVs and the role of EVs that are affected by Rab22a mutants in propelling tumor advancement. The dynamic interaction between Rab22a and EVs plays a significant role in the progression of tumors, and it can provide novel insights into the pathogenesis of cancers and the development of new therapeutic targets.

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Abbreviations

Rabs:

Ras-related GTP-binding proteins

EVs:

Extracellular vesicles

ER:

Endoplasmic reticulum

sEVs:

Small extracellular vesicles

MVs:

Microvesicles

DCs:

Dendritic cells

STING:

Stimulator of interferon genes

R-EVs:

Rab22a-induced extracellular vesicles

HIF:

Hypoxia-inducible factor

ARNT:

Aryl hydrocarbon receptor nuclear translocator

CBP:

CREB-binding protein

Pol II:

DNA polymerase II

HREs:

Hypoxia responsive elements

UTR:

Untranslated region

TNM:

Tumor node metastasis

NSCLC:

Non-small cell lung cancer

BC:

Breast cancer

CC:

Colon cancer

GTP:

Guanosine triphosphate

EEA:

Early endosomal antigen

MMP:

Matrix metalloproteinases

MCT-1:

Monocarboxylate transporter-1

CD44s:

CD44 standard splice isoform

STAT3:

Activator of transcription 3

MVE:

Multivesicular endosome

SmgGDS:

Small G protein guanine dissociation stimulator

ARMs:

Armadillo-repeat motifs

GEF:

Guanine exchange factor

GGTase-I:

Geranylgeranyltransferase-I

PMN:

Pre-metastatic niches

PYK2:

Proline-rich tyrosine kinase 2

ILVs:

Intraluminal vesicles

TAMs:

Tumor-associated macrophages

BMDCs:

Bone marrow-derived macrophages

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Acknowledgements

We thank all the subjects who participated in this study.

Funding

This work was supported by the Science and Technology Plan Project of Wenzhou (Grant Nos. Y20220389, Y20220045), Zhejiang Province Natural Science Foundation (Grant No. LTGY23H100001), and National Natural Science Foundation of China (Grant No. 81901660).

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Contributions

Writing, review, and editing, SHH, YXB; writing the first draft, SHH, YXB; final editing and proof reading, LJK, SG, CYH. All the authors have read and agreed to the published version of the article.

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Correspondence to Sheng Gao or Chunyan Hua.

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Huang, S., Bao, Y., Kong, L. et al. Insights into the complex interactions between Rab22a and extracellular vesicles in cancers. Inflamm. Res. 73, 99–110 (2024). https://doi.org/10.1007/s00011-023-01821-0

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  • DOI: https://doi.org/10.1007/s00011-023-01821-0

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