Gold nano-particles (AuNPs) carrying miR-326 targets PDK1/AKT/c-myc axis in hepatocellular carcinoma

Mo, Yichao; He, Longguang; Lai, Zeru; Wan, Zhiheng; Chen, Qinshou; Pan, Sibo; Li, Liangfu; Li, Dasheng; Huang, Jun; Xue, Fan; Che, Siyao

doi:10.1080/21691401.2018.1489266

Cited by 25 publications

(22 citation statements)

References 27 publications

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“…It is reported that the up-regulated miR-326 expression suppresses HCC cell growth and invasiveness as well as stimulates cell apoptosis in vitro [14]. Besides that, a prior study has verified that overexpression of miR-326 declined tumor growth in vivo [13]. A study has revealed that ectopic expressed miR-326 markedly attenuates cell growth, and suppresses cellular migration and invasiveness in non-small cell lung cancer cell lines [22].…”

Section: Discussionmentioning

confidence: 93%

“…A recent study has pointed out that miR-326 expression is declined in HCC tissues [20]. Another study has presented miR-326 expression is notably reduced in HCC cell lines and tissues and its down-regulation predicts a poor prognosis in HCC [13]. It is reported that miR-326 acts a tumor-suppression role and is greatly depressed in HCC cells [21].…”

Section: Discussionmentioning

confidence: 99%

“…MiR-NAs could act as either oncogenes or tumor inhibitors through modulating a large number of protein-encoded genes expression by means of mRNA degradation and translation blockage in a specific sequence [12]. A study has discussed that miR-326 suppresses HCC cell growth through disturbing cell-cycle progression as well as enhancing apoptosis, in addition suppresses cell invasion via decreasing the epithelial-mesenchymal transition phenotype [13]. Another study has reported that miR-326 could be a potential therapeutic target for HCC patients treatment [14].…”

Section: Introductionmentioning

confidence: 99%

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RETRACTED ARTICLE: M1 Macrophage-Derived Exosomal MicroRNA-326 Suppresses Hepatocellular Carcinoma Cell Progression Via Mediating NF-κB Signaling Pathway

Bai

et al. 2020

Nanoscale Res Lett

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Accumulating evidence has shown that microRNA (miR) derived from M1 macrophage-derived exosomes can regulate the progression of hepatocellular carcinoma (HCC). However, the effect of miR-326 derived from M1 macrophage-derived exosomes on HCC has not been reported. Therefore, the objective of the present study was to explore the mechanism of exosomal miR-326 from M1 macrophages in regulating HCC cell progression. RT-qPCR detected miR-326 expression in HCC cell lines. miR-326 expression in HCC was altered by transfection, and the effect of miR-326 on CD206 and NF-κB expression, cell proliferation, colony formation, migration, apoptosis and invasion was detected. Subsequently, exosomes were isolated from M1 macrophages. RT-qPCR identified miR-326 expression in M1 macrophage-derived exosomes. miR-326 expression in M1 macrophage-derived exosomes was changed by transfection. M1 macrophage-derived exosomes were co-cultured with HCC cells to figure out their effects on the biological progress of HCC cells. Finally, in vivo experiments were performed to verify the in vitro results. MiR-326 was decreased in HCC cells and enriched in M1 macrophage-derived exosomes. Up-regulating miR-326 would inhibit HCC cell proliferation, colony formation, migration, invasion, and CD206 and NF-κB expression and promoted apoptosis, and inhibited the growth of HCC tumors in vivo, while down-regulating miR-326 showed opposite effects. M1 macrophage-derived exosomes inhibited HCC cell proliferation, colony formation, migration, invasion, and CD206 and NF-κB expression and enhanced apoptosis, while overexpression of miR-326 enhanced the effect of M1 macrophage-derived exosomes on HCC cells. It is revealed that M1 macrophages-derived exosomal miR-326 suppresses proliferation, migration and invasion as well as advances apoptosis of HCC through down-regulating NF-κB expression.

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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RETRACTED ARTICLE: M1 Macrophage-Derived Exosomal MicroRNA-326 Suppresses Hepatocellular Carcinoma Cell Progression Via Mediating NF-κB Signaling Pathway

Bai

et al. 2020

Nanoscale Res Lett

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“…For instance, overexpression of miR-326 targets LIM and SH3 protein 1 to suppress HCC cell proliferation and invasion and promote apoptosis (48). Mo et al (49) demonstrated that miR-326 inhibits HCC tumor growth by blocking the Akt/c-Myc pathway through targeting of 3-phosphoinositide-dependent protein kinase 1. Upregulation of miR-326 reduces chemoresistance in numerous solid tumors, such as HCC (50), gastric cancer (51) and lung adenocarcinoma (52).…”

Section: Discussionmentioning

confidence: 99%

lncRNA PCAT6 facilitates cell proliferation and invasion via regulating the miR‑326/hnRNPA2B1 axis in liver cancer

et al. 2021

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Liver cancer is one of the most common malignant human tumors with the highest morbidity and mortality rates of all cancer types in China. Evidence suggests that long non-coding RNA prostate cancer-associated transcript 6 (PCAT6) plays an essential role in tumor progression. However, the roles and mechanism of PCAT6 in liver cancer remain unclear. The present study showed that the expression of PCAT6 and heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1) was upregulated in liver cancer tissues compared with non-cancerous tissues and were associated with poor overall survival time, whereas microRNA (miR)-326 expression was downregulated. Moreover, knockdown of PCAT6 significantly inhibited the proliferation and invasion of liver cancer cells in vitro and in vivo. A dual-luciferase reporter gene assay demonstrated that PCAT6 could bind to miR-326 and that hnRNPA2B1 was a direct target gene of miR-326. Mechanistically, silenced PCAT6 suppressed the malignant phenotype of liver cancer cells through upregulating the inhibitory effect of miR-326 on hnRNPA2B1 expression. Taken together, these data demonstrated that knockdown of PCAT6 inhibited liver cancer progression through regulation of the miR-326/hnRNPA2B1 axis, suggesting that PCAT6 functions as an oncogene and may be a useful biomarker for the future diagnosis and treatment of liver cancer.

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“…In short, miRNAs serve a critical role in CC progression (7). Other research has proposed that microRNA-326 (miR-326) makes a contribution to a variety of malignancies, including colorectal cancer (8), hepatocellular carcinoma (9), breast cancer (10), and endometrial carcinoma (11). Importantly, downregulation of miR-326 has been reported in CC tissues and cells (12).…”

Section: Introductionmentioning

confidence: 99%

miR-326 inhibits the cell proliferation and cancer stem cell-like property of cervical cancer in vitro and oncogenesis in vivo via targeting TCF4

Zhang¹,

He²,

Wang³

et al. 2020

Ann Transl Med

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Background: Cervical cancer ranks as one of the most prevalent female malignancies globally, and its treatment with new targets has been the focus of current research. The present study set out to investigate the function of microRNA-326 (miR-326) in vitro and in vivo and to verify the direct targeting of transcription factor 4 (TCF4) by miR-326. Methods: The detection of messenger RNA (mRNA) expressing miR-326 and TCF4 in cervical cancer cell lines and tumor samples was conducted using quantitative real-time polymerase chain (qRT-PCR). A dualluciferase reporter assay was carried out to detect the target relationship of miR-326 with TCF4. A Cell Counting Kit-8 (CCK-8) assay was employed to detect the effect of miR-326 on CasKi cell viability. Flow cytometry and western blotting were employed to examine the effects of miR-326 on cancer stem cell (CSC)like property. Tumor weight was measured in orthotopic xenograft mouse models. Immunohistochemistry was employed to analyze the protein expression levels of Ki-67, proliferating cell nuclear antigen (PCNA), CD44, and SRY-box 4 (SOX4). Result: Downregulation of the mRNA expression levels of miR-326 was observed in cervical cancer cell lines and tumor tissue, while the levels of TCF4 were upregulated. The dual-luciferase reporter assay revealed binding of miR-326 to the three prime untranslated region (3'-UTR) of TCF4. In vitro assays demonstrated that miR-326 inhibited CasKi cell proliferation through regulating TCF4. miR-326 also suppressed the CSC-like property of CasKi cells by targeting TCF4. Furthermore, the protein expression levels of cyclin D1, β-catenin, and c-Myc were decreased when miR-326 was added to TCF4-transfected cells. In vivo assays demonstrated that miR-326 inhibited tumor weight, growth, and the protein expression levels of Ki-67, PCNA, CD44, SOX4, and β-catenin.Conclusions: miR-326 acted in a tumor-suppressive manner through its regulation of TCF4, and has potential as a biomarker or therapeutic target for cervical cancer.

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Gold nano-particles (AuNPs) carrying miR-326 targets PDK1/AKT/c-myc axis in hepatocellular carcinoma

Cited by 25 publications

References 27 publications

RETRACTED ARTICLE: M1 Macrophage-Derived Exosomal MicroRNA-326 Suppresses Hepatocellular Carcinoma Cell Progression Via Mediating NF-κB Signaling Pathway

RETRACTED ARTICLE: M1 Macrophage-Derived Exosomal MicroRNA-326 Suppresses Hepatocellular Carcinoma Cell Progression Via Mediating NF-κB Signaling Pathway

lncRNA PCAT6 facilitates cell proliferation and invasion via regulating the miR‑326/hnRNPA2B1 axis in liver cancer

miR-326 inhibits the cell proliferation and cancer stem cell-like property of cervical cancer in vitro and oncogenesis in vivo via targeting TCF4

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