miR-26a regulates extracellular vesicle secretion from prostate cancer cells via targeting SHC4, PFDN4, and CHORDC1

Urabe, Fumihiko; Kosaka, Nobuyoshi; Sawa, Yurika; Yamamoto, Yusuke; Ito, Ken; Kimura, Takahiro; Egawa, Shin; Ochiya, Takahiro

doi:10.1126/sciadv.aay3051

Cited by 52 publications

(50 citation statements)

References 36 publications

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“…Furthermore, we searched some of the relevant public databases (GSE32448, 46602, and 55945) and found that miR‐1908 was downregulated in PCa tissues (Figure D). Intriguingly, based on this miRNA screening, we could not see any suppressive effect of EV secretion in 22Rv1 cells by miR‐26a, which was the most effective miRNA for suppression of EV secretion in PC3M 8 . Likewise, miR‐1908 was not an EV suppressive miRNA in PC3M cells (Figure E).…”

Section: Resultsmentioning

confidence: 82%

“…miRNAs through their dysregulated profiles function as regulators of both tumor progression and suppression in almost all types of cancer 7 . We have shown previously by comprehensive miRNA screening that miRNAs can regulate EV secretion in cancer cells 8 . In this study, 2 metastatic PCa cell lines, PC3 and PC3M, were employed; we found that miR‐26a regulates EV secretion in these cell lines through suppression of SHC4, PFDN4, and CHORDC1 8 .…”

Section: Introductionmentioning

confidence: 64%

“…Recently, we elucidated a novel pathway of EV biogenesis in PCa cell lines, PC3 and PC3M, using quantitative high‐throughput screening 8 . However, characteristics of EVs were different among PCa cell lines 9 .…”

Section: Discussionmentioning

confidence: 99%

“…Experiments were performed as described previously 8 . Briefly, high‐throughput miRNA screening (total 1728 miRNAs) was performed using the AccuTarget™ Human miRNA mimic library constructed based on the miRBase database v.21 (CosmoBio).…”

Section: Methodsmentioning

confidence: 99%

“…We have shown previously by comprehensive miRNA screening that miRNAs can regulate EV secretion in cancer cells 8 . In this study, 2 metastatic PCa cell lines, PC3 and PC3M, were employed; we found that miR‐26a regulates EV secretion in these cell lines through suppression of SHC4, PFDN4, and CHORDC1 8 . In addition, we have reported previously that the characteristics of EVs from PC3/PC3M and 22Rv1 cells differ even though PC3/PC3M and 22Rv1 are both castration‐resistant prostate cancer (CRPC) cell lines 9 .…”

Section: Introductionmentioning

confidence: 99%

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The miR‐1908/SRM regulatory axis contributes to extracellular vesicle secretion in prostate cancer

et al. 2020

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Targeting extracellular vesicle (EV) secretion can have potential clinical implications for cancer therapy, however the precise regulatory mechanisms of EV secretion are not fully understood. Recently, we have shown a novel pathway of EV biogenesis in PCa cell lines, PC3 and PC3M. However, as the characteristics of EVs are divergent even among PCa cell lines, we hypothesized that other pathways or common regulatory pathways of EV biogenesis still exist. Here, we performed quantitative high‐throughput screening to determine the key regulatory genes involved in EV biogenesis in 22Rv1 cells, which secrete a different type of EVs. In total, 1728 miRNAs were screened and miR‐1908 was selected as the potential miRNA regulating EV biogenesis in 22Rv1 cells. Subsequently, we investigated target genes of miR‐1908 using siRNA screening and identified that spermidine synthase (SRM) was the key regulator of EV secretion in 22Rv1 cells. Attenuation of SRM expression significantly inhibited secretion of EVs in 22Rv1 cells, and overexpression of SRM was confirmed in PCa tissues. Furthermore, we found that the number of endosome compartments was increased in cellular cytoplasm after knockdown of the SRM gene. In conclusion, our results showed that miR‐1908‐mediated regulation of SRM can control secretion of EVs in PCa. In addition, these data suggested that the EV secretion pathway was dependent on cellular characteristics.

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Section: Resultsmentioning

confidence: 82%

Section: Introductionmentioning

confidence: 64%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The miR‐1908/SRM regulatory axis contributes to extracellular vesicle secretion in prostate cancer

et al. 2020

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Exosomal miR‐1470 is a diagnostic biomarker and promotes cell proliferation and metastasis in colorectal cancer

Wu,

Zhang,

Lin

et al. 2024

Cancer Medicine

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BackgroundIn recent years,the lack of specific markers for the diagnosis of colorectal cancer has led to an upward trend in both morbidity and mortality from this condition. There is an urgent need to identify molecular biomarkers that contribute to early cancer detection. This study aimed to identify specific exosomal microRNAs that hold potential as diagnostic biomarkers for CRC.MethodsWe screened for differentially expressed miRNAs using the CRC exosome dataset GSE39833. To validate the results in the public database, we collected serum from 168 CRC patients and 168 healthy volunteers. The expression levels of exosomal miR‐1470 in healthy volunteers and CRC patients were analyzed using qRT‐PCR. To evaluate the diagnostic potential of the selected miR‐1470 in distinguishing CRC patients from healthy controls, we analyzed its receiver operating characteristic curve. To explore the biological functions of miR‐1470 in CRC cell lines, we detected the miR‐1470's ability to regulate the growth and metastasis of CRC cells by CCK8, transwell and other assays after transfection of miR‐1470 in SW480, HCT‐116 cells.ResultsExosomal miR‐1470 exhibited significant up‐regulation in CRC patients compared to healthy volunteers. The ROC curve analysis revealed an area under the curve (AUC) of 0.74 (95% confidence interval: 0.6876–0.7920) for exosomal miR‐1470, indicating its potential as a diagnostic biomarker. Furthermore, the expression level of miR‐1470 in CRC patients showed correlations with age, metastasis, and HDL content. We overexpressed miR‐1470 in CRC cell lines. CCK8 proliferation assay showed that miR‐1470 promoted the proliferation ability of SW480 and HCT‐116 cells. Transwell assay showed that miR‐1470 promoted the migration and invasion ability of SW480 and HCT‐116 cells.ConclusionThis suggested that non‐invasive diagnosis of CRC is possible by detecting the level of miR‐1470 in exosomes, which has important implications for early detection and treatment of this disease.

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LINC00240 knockdown inhibits nasopharyngeal carcinoma progress by targeting miR‐26a‐5p

Chen

Jing

et al. 2022

Clinical Laboratory Analysis

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Objective: This study intended to explore the regulatory functions of LINC00240 on nasopharyngeal carcinoma (NPC).Methods: MiR-26a-5p inhibitor, mimic, and siLINC00240 were transfected into NPC cells. QRT-PCR was employed to assess miR-26a-5p and LINC00240 expressions.The targeting relationship of LINC00240 and miR-26a-5p was analyzed through dual luciferase reporter and RNA immunoprecipitation assay. Cell counting kit-8 assay, colony formation assay, flow cytometry assay, wound healing assay, Transwell assay and in vitro angiogenesis assay were adopted for the evaluation of the effects of LINC00240 or miR-26a-5p and LINC00240 on NPC cells regarding cell proliferation, apoptosis and cycle, migration, invasion, and angiogenesis. EZH2, cell cycle, and epithelial-mesenchymal transition (EMT)-related protein expression was tested through Western blot.Results: LINC00240 had a high expression in NPC tissues and cell lines. Silenced LINC00240 significantly suppressed the 5-8F and HK1 cell proliferation, invasion, migration, and angiogenesis, but raised cell apoptosis, and cells were blocked in G0/G1 phase. MiR-26a-5p was a target of LINC00240. MiR-26a-5p upregulation suppressed the NPC cell proliferation, migration, invasion, angiogenesis, N-cadherin and EZH2 expression, while it elevated apoptosis and p21, p27 and E-cadherin expressions, whereas miR-26a-5p downregulation performed conversely. LINC00240 knockdown partially offset the effects of miR-26a-5p downregulation on cell proliferation, migration, invasion, angiogenesis, apoptosis, and EZH2. Conclusion:LINC00240 knockdown restrained cell proliferation, invasion, migration, and angiogenesis, while it advanced apoptosis via miR-26a-5p in NPC by EZH2 inhibition.

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miR-26a regulates extracellular vesicle secretion from prostate cancer cells via targeting SHC4, PFDN4, and CHORDC1

Cited by 52 publications

References 36 publications

The miR‐1908/SRM regulatory axis contributes to extracellular vesicle secretion in prostate cancer

The miR‐1908/SRM regulatory axis contributes to extracellular vesicle secretion in prostate cancer

Exosomal miR‐1470 is a diagnostic biomarker and promotes cell proliferation and metastasis in colorectal cancer

LINC00240 knockdown inhibits nasopharyngeal carcinoma progress by targeting miR‐26a‐5p

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