miR-148a-3p inhibits the proliferation and migration of bladder cancer <i>via</i> regulating the expression of ROCK-1

Xu, Chao; Zhou, Guanwen; Sun, Zhuang; Zhang, Zhaocun; Zhao, Haifeng; Jiang, Xianzhou

doi:10.7717/peerj.12724

Cited by 9 publications

(5 citation statements)

References 24 publications

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“…RhoA regulates the epithelial barrier not only through ROCK alone but also scaffold proteins such as rhophilin, rhotekin, kinectin, and mDia, and serine/threonine protein kinases such as PKN and citron kinase . ROCK is also regulated by Piezo1, Coronin1A/B, and miR-148a-3p, among others. − Neither Rosin nor Y-27632 alone could indicate that DON-mediated damage to the intestinal epithelial barrier is through the RhoA/ROCK pathway. So for the accuracy of the study, we used both Rosin and Y-27632 separately.…”

Section: Discussionmentioning

confidence: 99%

Deoxynivalenol Induces Intestinal Epithelial Barrier Damage through RhoA/ROCK Pathway-Mediated Apoptosis and F-Actin-Associated Tight Junction Disruption

Miao,

Wu,

Sun

et al. 2024

J. Agric. Food Chem.

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Deoxynivalenol (DON) poses a serious global food safety risk due to its high toxicity and contamination rate. It disrupts the intestinal epithelial barrier, allowing exogenous toxins to enter the circulation and resulting in sepsis and systemic toxicity. In this research, 32 male Kunming mice and Porcine Small Intestinal Epithelial (IPEC-J2) cells were treated with DON at 0−4.8 mg/kg (7 d) and 0−12 μM (24 h), respectively. Histopathological results revealed that DON disrupted the intestinal epithelial barrier, causing apoptosis and tight junction (TJ) injury. Immunofluorescence and protein expression results showed that DON-induced p53-dependent mitochondrial pathway apoptosis and fibrillar actin (F-actin)-associated TJ injury and that the RhoA/ ROCK pathway were activated in mice jejunal tissue and IPEC-J2 cells. Pretreatment with RhoA or ROCK inhibitors (Rosin or Y-27632) maintained DON-induced apoptosis and F-actin-associated TJ injury in IPEC-J2 cells. Thus, DON induces damage to the intestinal epithelial barrier through the RhoA/ROCK pathway-mediated apoptosis and F-actin-associated TJ disruption.

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Section: Discussionmentioning

confidence: 99%

Deoxynivalenol Induces Intestinal Epithelial Barrier Damage through RhoA/ROCK Pathway-Mediated Apoptosis and F-Actin-Associated Tight Junction Disruption

Miao,

Wu,

Sun

et al. 2024

J. Agric. Food Chem.

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“…EGFR is reported to be over-expressed in up to 85% of SACC, making it a therapeutic target of interest [39]. Recent studies have shown that EGFR is abnormally over-expressed in metastatic SACC and is a key regulatory molecule for SACC metastasis [40]. Prior studies have targeted the EGFR pathway via numerous therapeutic agents including ge tinib [41], cetuximab [42], and lapatinib [43] without meaningful response rates.…”

Section: Discussionmentioning

confidence: 99%

TAMs-derived exosomal Meg8 promotes the EMT and metastasis of SACC by regulating EGFR through sponge absorption of miR-148a-3p

Gao,

Wang,

Shi

et al. 2024

Preprint

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Tumor-associated macrophages (TAMs) infiltrate extensively in salivary adenoid cystic carcinoma (SACC) tissues. Our previous study found that TAMs were significantly associated with the tumor metastasis and poor patients’ prognosis. However, the role and molecular mechanism of TAMs in SACC metastasis are still to be elucidated. Present study found that TAMs-derived exosomes can be internalized by SACC cells, initiating the epithelial-mesenchymal transition (EMT) process of SACC cells. TAMs-derived exosomal RNA sequencing and metastasis-related SACC tissues RNA sequencing suggested that Lnc-Meg8 was involved in TAMs-SACC interaction. RNA fluorescent in situ hybridization, RNA immunoprecipitation, and other in vitro assays revealed that TAMs-derived exosomes transferred Lnc-Meg8 to SACC cells, which promoted EGFR expression via sponge absorption of miR-148a-3p, thus promoting the EMT process of SACC cells. In vivo fluorescence imaging and immunohistochemical staining confirmed that inhibition of TAMs-derived exosomal Meg8 significantly improved the therapeutic efficacy of EGFR inhibitor cetuximab on the EMT and metastasis of SACC cells. In summary, our results demonstrated that the TAMs-derived exosomes promoted the EMT process of SACC cells via the Lnc-Meg8/miR-148a-3p/EGFR molecular axis. Blocking exosomal Lnc-Meg8 of TAMs may be a potential therapeutic strategy for SACC.

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“…Our data advise that circFTO regulates NSCLC proliferation and migration via sponge miR-148a-3p, which could inhibit tumorigenesis development. Xu et al reported that miR-148a-3p suppresses bladder cancer proliferation and migration via regulating Roc-1 expression [ 35 ]. Zeng et al found that circANKS1B regulates breast cancer by promoting the transcription factor UF1 expression via the sponge miR-148a-3p [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

circFTO from M2 macrophage-derived small extracellular vesicles (sEV) enhances NSCLC malignancy by regulation miR-148a-3pPDK4 axis

Liu,

Xu,

Jin

et al. 2024

Cancer Immunol Immunother

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Background Accumulation studies found that tumor-associated macrophages (TAMs) are a predominant cell in tumor microenvironment (TME), which function essentially during tumor progression. By releasing bioactive molecules, including circRNA, small extracellular vesicles (sEV) modulate immune cell functions in the TME, thereby affecting non-small cell lung cancer (NSCLC) progression. Nevertheless, biology functions and molecular mechanisms of M2 macrophage-derived sEV circRNAs in NSCLC are unclear. Methods Cellular experiments were conducted to verify the M2 macrophage-derived sEV (M2-EV) roles in NSCLC. Differential circRNA expression in M0 and M2-EV was validated by RNA sequencing. circFTO expression in NSCLC patients and cells was investigated via real-time PCR and FISH. The biological mechanism of circFTO in NSCLC was validated by experiments. Our team isolated sEV from M2 macrophages (M2Ms) and found that M2-EV treatment promoted NSCLC CP, migration, and glycolysis. Results High-throughput sequencing found that circFTO was highly enriched in M2-EV. FISH and RT-qPCR confirmed that circFTO expression incremented in NSCLC tissues and cell lines. Clinical studies confirmed that high circFTO expression correlated negatively with NSCLC patient survival. Luciferase reporter analysis confirmed that miR-148a-3p and PDK4 were downstream targets of circFTO. circFTO knockdown inhibited NSCLC cell growth and metastasis in in vivo experiments. Downregulating miR-148a-3p or overexpressing PDK4 restored the malignancy of NSCLC, including proliferation, migration, and aerobic glycolysis after circFTO silencing. Conclusion The study found that circFTO from M2-EV promoted NSCLC cell progression and glycolysis through miR-148a-3p/PDK4 axis. circFTO is a promising prognostic and diagnostic NSCLC biomarker and has the potential to be a candidate NSCLC therapy target.

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miR-148a-3p inhibits the proliferation and migration of bladder cancer via regulating the expression of ROCK-1

Cited by 9 publications

References 24 publications

Deoxynivalenol Induces Intestinal Epithelial Barrier Damage through RhoA/ROCK Pathway-Mediated Apoptosis and F-Actin-Associated Tight Junction Disruption

Deoxynivalenol Induces Intestinal Epithelial Barrier Damage through RhoA/ROCK Pathway-Mediated Apoptosis and F-Actin-Associated Tight Junction Disruption

TAMs-derived exosomal Meg8 promotes the EMT and metastasis of SACC by regulating EGFR through sponge absorption of miR-148a-3p

circFTO from M2 macrophage-derived small extracellular vesicles (sEV) enhances NSCLC malignancy by regulation miR-148a-3pPDK4 axis

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