miR-21 overexpression

Our findings indicate that miR-21 post-transcriptionally down-regulates the expression of RECK to promote cell proliferation and cell migration inhibition in cervical cancer cell survival. Therefore, miR-21 and RECK may be potential therapeutic targets in gene therapy for cervical cancer.

Furthermore, the glucose oxidase-like activity of the AuNPs accelerates intracellular glucose consumption, promoting cancer cell starvation. The engineered AuNPs@anti-miR-21/siGlut1 complex inhibits cancer cell proliferation, xenograft tumor growth and promotes apoptosis through glucose starvation and ROS cascade signaling, underscoring its potential as an effective therapeutic strategy for lung cancer.

Conversely, by modulating various mechanisms and oncogenic signaling pathways, their overexpression has been linked with preventing tumor formation and development. This review highlights the significance of these regulatory pathways in cancer and their potential for use in cancer therapy as diagnostic and prognostic markers.

Moreover, EVs isolated from the CSF of LM patients containing miR-21 could enhance the cell proliferation and MTX resistance of recipient cells. These results indicate that miR-21 can be transferred from cell-to-cell via EVs and potentially modulate MTX sensitivity, suggesting that miR-21 in CSF EVs may be a prognostic and therapeutic target for overcoming MTX resistance in patients with NSCLC-LM.

In vivo xenograft experiments further confirmed that RAB5A knockdown TNBC cells exhibited reduced tumor formation and impaired tumor-associated macrophage recruitment. These studies shed light on the potential underlying mechanism of RAB5A-mediated macrophage polarization in an exosomal miR-21-dependent manner and provide an experimental basis for the development of RAB5A- or exosome-based tumor therapeutic strategies.

CRC cell-EV-miR-21 annulled the suppression effects of GA on macrophage M2 polarization. GA suppressed macrophage M2 polarization by lessening tumor cell derived-EV-shuttled miR-21, thereby weakening CRC invasion/metastasis.

Conversely, miR-21-5p inhibition or SPRY1 overexpression enhanced MV's effect on inflammatory responses in LPS-exposed RAW 264.7 cells. Therefore, the significant protective effect of mogroside V on inflammation response is related to the downregulation of miR-21-5p and upregulation of SPRY1 in vitro and in vivo, MiR-21-5p/SPRY1 may be novel therapeutic targets of MV for anti-inflammation treatment.

CAF-EVs promoted GEM resistance in PC via the miR-21/RAS/ATK/ERK pathway in vivo. Hypoxia promoted CAFs to secrete high-level miR-21 EVs through the HIF-1α/miR-21 axis, and activated the miR-21/RAS/AKT/ERK pathway via EVs to trigger stemness maintenance and GEM resistance in PC.

CPT and TanIIA play a regulatory role in regulating tight junction proteins (Occludin and ZO1), and Occludin mRNA and protein levels were reduced in an in vitro miR-21-5p overexpression A549 cell model. The mechanisms may be related to the reduction of miR-21-5p expression to increase the level of promoted tight junction protein expression for the purpose of inhibiting proliferation and invasion of NSCLC.

Our findings suggest that this developed system offers a simple and sensitive approach for detecting endogenous miRNAs in plasma, showing its potential utility in disease diagnostics. To our knowledge, this is the first study to utilize CE-LIF for plasma miRNA detection.

Examining PDCD4 and miR-21 transcript levels may help detect the transition from OED to OSCC. This work suggests that PDCD4 and miR-21 expression levels in liquid biopsies may be biomarkers for OED monitoring in the future.

Furthermore, we demonstrate that miR-21 can be used as a target against proliferation control because its knockout is equivalent to PTEN overexpression. We think the findings can be used to motivate new strategies for MCF-7 strain proliferation control.

This pilot study provides a novel panel of saliva and serum miRNAs associated with oral cancer. Further validation as a potential useful index of oral cancer, particularly miR-21 in smokers and early-stage OSCC is warranted.

This study is the highest level of evidence presently available in diagnosing HNSCC. This PRISMA meta-analysis indicated that the pooled results were robust, confirming the oncogenic potential of miR-21 that could be used successfully as a screening biomarker in HNSCC patients. Specifically, the overexpression of miR-21 in these patients presents a worse survival outcome.

Moreover, there was a gradual decrease in dual-color AIENP fluorescence as the HepG2 cell concentration of AA (0-500 μM) and stimulation time (0-12 h) increased, making it possible to simultaneously image AA and AA-induced miR-21. The findings of this work are valuable for revealing the cytotoxic mechanism of AA.

Exosomal miR-21-5p in HCC cells can affect the development of HCC cells by regulating SP1/XBP1 and promoting the M2 polarization of TAMs, thereby affecting the adverse prognostic response of HCC patients.

Results reinforce the concept of interaction between tumor cells and inflammatory cells within the TME, with a central role of IL-6 and TNF-α. Since the upregulation of miR-21 reflects the gene overexpression of interleukins and the high proliferation index of tumor cells, this miRNA may be considered a biomarker with prognostic value in CMTs.

Moreover, miR-21-inhibit could hinder cell viability, invasion, and glycolysis triggered by overexpression of PFKFB2 in brain glioma cells. miR-21-5p level is elevated in brain glioma and can impede brain glioma cell growth via regulating the glycolysis mediated by PFKFB2, thus is a potential target of treating brain glioma.

Results also indicate that miR-21-5p regulated lidocaine-induced injury through targeting PDCD4. BMSC-exos protected SH-SY5Y cells against lidocaine induced apoptosis through miR-21-5p by targeting PDCD4, which may develop new strategy in the management of lidocaine-induced neurotoxicity.

Clinicopathological analysis revealed correlations between decreased ASPP2 expression and higher HPGC risk and poor prognosis. In summary, the discovery of H. pylori-induced antiapoptosis via miR-21-mediated suppression of ASPP2/CHOP-mediated signaling provides a novel perspective for developing HPGC management and treatment.

Furthermore, we demonstrated that miR-21-5p inhibits glioma proliferation, migration, and invasion by targeting S100A10. This study showed S100A10 was a new prognostic predictor among glioma patients and provided new insights into the pathogenesis of gliomas, suggesting that miR-21-5p /S100A10 axis may serve as a valuable therapeutic target for glioma.

Moreover, miR-21 inhibition significantly enhanced cisplatin- or radiation-induced apoptosis. Western blot analysis suggested the programmed cell death 4 protein as a potential target of miR-21 in relation to apoptosis. In conclusion, this study provides new insights into the role of miR-21 as a predictive biomarker for HNSCC treated with chemoradiotherapy and suggests a potential target to improve the effects of chemoradiotherapy against HNSCC.

Our results showed that miR-21 can transform NFs into CAFs, and that CAF exosomes promote angiogenesis by carrying miR-21 into MMECs. Therefore, CAF-derived exosomal miR-21 may serve as a novel diagnostic biomarker and therapeutic target for MM.

miR-21-5p promotes deterioration and sorafenib resistance in hepatocellular carcinoma by upregulating autophagy levels. Knockdown of miR-21-5p inhibits the development of sorafenib-resistant tumors by USP24-mediated SIRT7 ubiquitination.

This study constructed the miRNA-hub gene network, which provides novel insights into the PDAC progression. Although further research is required, our results offer clues for new potential prognostic markers and therapeutic targets of PDAC.

This study suggests that circ_001859 may inhibit the proliferation, invasion and EMT of pancreatic cancer through the miR-21-5p/SLC38A2 pathway.

In summary, Zhigancao Decoction, a traditional Chinese medicine preparation, improves doxorubicin-inducedmyocardial apoptosis by modulating proinflammatory cytokines expression via the miRNA-21 / TLR4 / MAPK pathway. Chemotherapy, Doxorubicin, Chemotherapy toxicity, Anthracycline

Our results showed that OL-FS13 alleviated OGD/R and CI/R by inhibiting miR-21-3p to activate the CAMKK2/AMPK/Nrf-2 axis.

Taken together, GAS5 was involved in gemcitabine resistance in pancreatic carcinoma and possibly through regulating miR-21, and subsequent cell proliferation, apoptosis and expression of multidrug resistant transporters.

MiRNAs: High miR-21 expression predicted poor OS of BC, high miR-222 expression led to poor OS of BC, high miR-155 expression predicted poor progression-free survival (PFS) of BC, high miR-143 expression caused poor PFS of BC, low miR-214 expression could result in poor recurrence-free survival (RFS) of BC. High circ-ZFR, lnc-TUG1, miR-222 and miR-21 expression was correlated with poor OS of BC; high miR-155 and miR-143 expression predicted poor PFS of BC; low lnc-GAS5 expression predicted poor OS of BC; low miR-214 expression predicted poor RFS of BC.

Benefiting from the multiple functional improvements and synergism between Gem and miR-21i, the miR-21i@HA-Gem-SS-P12 nanoprodrugs displayed superior tumor inhibition in PDAC in vitro and in vivo. This study established an effective stimuli-responsive nanoprodrug strategy for cooperative treatment with small molecule agents and nucleotide modulators in PDAC. .

Therefore, GABPB1-IT1 may upregulate PTEN by sponging miR-21 in ccRCC to inhibit cancer cell proliferation. Our study characterized a novel GABPB1-IT1/miR-21/PTEN axis in ccRCC.

Erastin, an inducer of ferroptosis, attenuated the repressive influence of miR-21-5p on ferroptosis in HCC cells. In summary, this study demonstrates that miR-21-5p inhibits the ferroptosis of HCC cells by regulating the AKT/mTOR signaling pathway through MELK.

Taken together, tumor-derived miR-21-5p promote the malignant advance of HCC, which mediated intercellular crosstalk between tumor cells and macrophages. Targeting M2-like TAMs and intercepting their associated signaling pathways would provide potentially specific and novel therapeutic approaches for HCC treatment.

In order to achieve a better tumor control, we tested the combined treatments with miR-21-5p inhibitor and PARP1 inhibitor (Olaparib) on SAS cells, which resulted in a synergistic effect in inhibition of the repair of DNA double strand breaks. The residual 53BP1 foci after 2Gy X-ray irradiation was increased 1.45±0.06 folder more when inhibiting both miR-21-5p and PARP1, while the colony-forming capacity of irradiated SAS cells was decreased by 39.55±5.89% (p<0.0001) in the same conditions. This work provided novel insights on the molecular mechanism of miR-21-5p regulated cell response to radiotherapy, which may give rise to potential therapeutic strategy for treatment of advanced OSCC.

In addition, a better progression-free survival (PFS) is associated with MGMT methylation and GTR but not with MGMT IHC and miRNA expression. In conclusion, our data reinforce the clinical relevance of miRNA expression as an additional marker to predict efficacy of chemoradiation in GBM.

This study presents evidence that hypoxia is a key contributor to the over-expression of miR-21 in prostate tumours, which can subsequently promote prostate cancer progression by suppressing RHOB expression. We propose that miR-21 has good potential as a clinically useful diagnostic and prognostic biomarker of hypoxia and prostate cancer.

miR-21-5p is negatively correlated with DSCR9 and BTG2. In conclusion, the DSCR9/miR-21-5p/BTG2 axis modulates pancreatic cancer proliferation, invasion, and gemcitabine resistance.

The overexpression of miR-21 and miR-191 in patients with DLBCL is related to high clinical stage.

The results suggest that the co-micelles of AMO21c and T7c may be an efficient delivery system into a brain tumor through intranasal administration.

In comparison to the patients with low miR-21, the patients with high miR-21 expression had significant increase in OS as they benefit from gemcitabine-based adjuvant chemotherapy (Glasgow 16.5 months [with chemotherapy] vs 10.5 months [without chemotherapy]); Sydney 25.0 vs 10.6; ICGC 25.2 vs 11.9. These results indicated that miR-21 is a predictor of survival, prompting prospective trials. Evaluation of miR-21 offers new opportunities for the stratification of patients with PDAC and might facilitate the implementation of clinical management and therapeutic interventions for this devastating disease.