CRIP1 supports the growth and migration of AML-M5 subtype cells by activating Wnt/β-catenin pathway

Deng, Xiaoling; Zeng, Yanmei; Qiu, Xiaofen; Zhong, Minghua; Xiong, Xiujuan; Mansheng, Luo; Zhang, Jingdong; Chen, X.

doi:10.1016/j.leukres.2023.107312

Leukemia Research

2023

DOI: 10.1016/j.leukres.2023.107312

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CRIP1 supports the growth and migration of AML-M5 subtype cells by activating Wnt/β-catenin pathway

Xiaoling Deng

Yanmei Zeng

Xiaofen Qiu

et al.

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2024

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Cited by 3 publications

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Cancer‐associated fibroblasts‐secreted exosomal miR‐92a‐3p promotes tumor growth and stemness in hepatocellular carcinoma through activation of Wnt/β‐catenin signaling pathway by suppressing AXIN1

Su,

Lu,

Zhang

et al. 2024

Journal Cellular Physiology

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Cancer‐associated fibroblasts (CAFs) are a major cellular component in the tumor microenvironment and have been shown to exhibit protumorigenic effects in hepatocellular carcinoma (HCC). This study aimed to delve into the mechanisms underlying the tumor‐promoting effects of CAFs in HCC. Small RNA sequencing was conducted to screen differential expressed microRNAs in exosomes derived from CAFs and normal fibroblasts (NFs). The miR‐92a‐3p expression was then measured using reverse transcriptase quantitative real‐time PCR in CAFs, NFs, CAFs‐derived exosomes (CAFs‐Exo), and NF‐derived exosomes (NFs‐Exo). Compared to NFs or NF‐Exo, CAFs and CAFs‐Exo significantly promoted HCC cell proliferation, migration, and stemness. Additionally, compared to NFs or NF‐Exo, miR‐92a‐3p level was notably higher in CAFs and CAFs‐Exo, respectively. Exosomal miR‐92a‐3p was found to enhance HCC cell proliferation, migration, and stemness. Meanwhile, AXIN1 was targeted by miR‐92a‐3p. Exosomal miR‐92a‐3p could activate β‐catenin/CD44 signaling in HCC cells by inhibiting AXIN1 messenger RNA. Furthermore, in vivo studies verified that exosomal miR‐92a‐3p notably promoted tumor growth and stemness through targeting AXIN1/β‐catenin axis. Collectively, CAFs secreted exosomal miR‐92a‐3p was capable of promoting growth and stemness in HCC through activation of Wnt/β‐catenin signaling pathway by suppressing AXIN1. Therefore, targeting CAFs‐derived miR‐92a‐3p may be a potential strategy for treating HCC.

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Cancer‐associated fibroblasts‐secreted exosomal miR‐92a‐3p promotes tumor growth and stemness in hepatocellular carcinoma through activation of Wnt/β‐catenin signaling pathway by suppressing AXIN1

Su,

Lu,

Zhang

et al. 2024

Journal Cellular Physiology

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CRIP1 regulates osteogenic differentiation of bone marrow stromal cells and pre-osteoblasts via the Wnt signaling pathway

Chen,

Jin,

Lian

et al. 2024

Biochemical and Biophysical Research Communications

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CRIP1 involves the pathogenesis of multiple myeloma via dual-regulation of proteasome and autophagy

Tang,

Yu,

Sun

et al. 2024

eBioMedicine

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CRIP1 supports the growth and migration of AML-M5 subtype cells by activating Wnt/β-catenin pathway

Cited by 3 publications

References 27 publications

Cancer‐associated fibroblasts‐secreted exosomal miR‐92a‐3p promotes tumor growth and stemness in hepatocellular carcinoma through activation of Wnt/β‐catenin signaling pathway by suppressing AXIN1

Cancer‐associated fibroblasts‐secreted exosomal miR‐92a‐3p promotes tumor growth and stemness in hepatocellular carcinoma through activation of Wnt/β‐catenin signaling pathway by suppressing AXIN1

CRIP1 regulates osteogenic differentiation of bone marrow stromal cells and pre-osteoblasts via the Wnt signaling pathway

CRIP1 involves the pathogenesis of multiple myeloma via dual-regulation of proteasome and autophagy

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