ARPC5 is transcriptionally activated by KLF4, and promotes cell migration and invasion in prostate cancer via up-regulating ADAM17

Qu, Genyi; Duan, Hongtao; Tang, Chaowei; Yang, Guang; Chen, Dan; Xu, Yong

doi:10.1007/s10495-023-01827-3

Cited by 3 publications

(2 citation statements)

References 40 publications

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“…This mechanism contributes to the enhancement of transendothelial migration and lung metastasis in colorectal cancer. Building upon previous studies [48,49], we have elucidated a regulatory pathway, as illustrated in Figure 7. Our conclusions are as follows: (i) The overexpression of BAP31 leads to a decrease in both precursors and matures of the miR-206/133b cluster in CRC cells; (ii) miR-206 directly targets CDC42, while miR-133b targets ARPC5, facilitating the transendothelial migration of CRC cells; (iii) The regulation of the miR-206/133b cluster in BAP31-overexpressing CRC cells depends on the translocation of HOXD10 from the cytoplasm to the nucleus, and disrupting this regulatory axis with HOXD10 significantly weakens the phenotype of transendothelial migration and metastasis in BAP31-overexpressing induced CRC cells.…”

Section: Discussionmentioning

confidence: 99%

BAP31-Mediated miR-206/133b Cluster Promotes Transendothelial Migration and Metastasis of Colorectal Cancer

Zhang,

Wang,

et al. 2023

IJMS

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Dysregulated B cell receptor-associated protein 31 (BAP31) plays a crucial role in tumor progression. This study aimed to investigate the functions and molecular mechanism of BAP31 on the miR-206/133b cluster in colorectal cancer (CRC). qPCR was conducted to detect miRNA and mRNA levels in tissues and cells. Western blot assays were used to assess the levels of biomarkers and targets, as well as the levels of BAP31 and HOXD10. Wound healing, coculture and transwell assays were conducted to assess the transendothelial migration abilities of CRC cells. A luciferase assay was employed to assess miRNA binding effects on targets, as well as the initiating transcription effect of genomic fragments. Tumor growth and lung metastatic models were established through an in vivo animal study. BAP31 overexpression in CRC cells led to a reduction in the expression of the miR-206/133b cluster. The expression of the miR-206/133b cluster was correlated with the transendothelial migration capability of CRC cells. The miR-206/133b cluster was found to directly regulate cell division cycle 42 (CDC42) and actin-related protein 2/3 complex subunit 5 (ARPC5) in the tight junction pathway (hsa04530). Moreover, a potential transcription regulator of the miR-206/133b cluster was also found to be Homeobox D10 (HOXD10). We further elucidated the molecular mechanisms and functional mechanisms of BAP31’s regulatory role in the expression levels of the miR-206/133b cluster by inhibiting HOXD10 translocation from the cytoplasm to the nucleus. In conclusion, this study provides valuable insights into how BAP31 regulates the transcription of the miR-206/133b cluster and how BAP31-related lung metastases arise in CRC.

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Section: Discussionmentioning

confidence: 99%

BAP31-Mediated miR-206/133b Cluster Promotes Transendothelial Migration and Metastasis of Colorectal Cancer

Zhang,

Wang,

et al. 2023

IJMS

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“…Assessing patients’ clinical prognosis can be achieved by examining the combination of ARPC1B with PTEN or ERG ( Gamallat et al, 2022 ). Krüppel-like factor 4 (KLF4) acts as a transcriptional activator of ARPC5, promoting PCa progression through the activation and upregulation of ARPC5 via the Notch and Wnt pathways ( Qu et al, 2023 ). The aforementioned studies provide initial insights into the significant roles of ARPC1A, ARPC1B, and ARPC5 within the Arp2/3 complex in PCa, underscoring their importance in cell migration and invasion.…”

Section: Actin Filament Nucleation In Pcamentioning

confidence: 99%

Role of actin-binding proteins in prostate cancer

Fu,

Yu,

Zou

et al. 2024

Front. Cell Dev. Biol.

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The molecular mechanisms driving the onset and metastasis of prostate cancer remain poorly understood. Actin, under the control of actin-binding proteins (ABPs), plays a crucial role in shaping the cellular cytoskeleton, which in turn supports the morphological alterations in normal cells, as well as the invasive spread of tumor cells. Previous research indicates that ABPs of various types serve distinct functions, and any disruptions in their activities could predispose individuals to prostate cancer. These ABPs are intricately implicated in the initiation and advancement of prostate cancer through a complex array of intracellular processes, such as severing, linking, nucleating, inducing branching, assembling, facilitating actin filament elongation, terminating elongation, and promoting actin molecule aggregation. As such, this review synthesizes existing literature on several ABPs linked to prostate cancer, including cofilin, filamin A, and fascin, with the aim of shedding light on the molecular mechanisms through which ABPs influence prostate cancer development and identifying potential therapeutic targets. Ultimately, this comprehensive examination seeks to contribute to the understanding and management of prostate diseases.

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