MALAT1 overexpression

Our findings suggest that MALAT1 suppresses monocyte-EC interactions by targeting miR-30b-5p and enhancing ATG5-mediated endothelial autophagy. These data imply that MALAT1 may play a protective role at the early stages of the atherosclerotic process.

MALAT1 in human umbilical cord mesenchymal stem cells expedited foot ulcer healing in diabetic rats, particularly in age-associated diabetes, through miR-142 sponge activity. These findings offer insights for novel therapeutic strategies targeting elderly diabetic foot ulcers, emphasizing exogenous stem cell transplantation's potential in effective DFU treatment for the elderly.

The contours of our findings sketch a compelling landscape wherein HR-HPV infection, TP53 polymorphism, and MALAT1 expression intertwine significantly in cervical cancer. The voyage ahead entails delving deeper into molecular underpinnings to decipher MALAT1's nuanced role and its dance with TP53 within HPV-associated cervical carcinogenesis. This expedition promises insights that may engender targeted therapeutic interventions and bespoke prognostic markers, tailored to the realm of HR-HPV-related cervical cancer.

As expected, DNMT1 overexpression could remarkably inhibit TNBC stemness and tumorigenesis, which was eliminated by MALAT1 overexpression. MALAT1 downregulated DNMT1 by miR-137/BCL11A pathway to enhance TNBC stemness and tumorigenesis; meanwhile, DNMT1/MALAT1 formed a positive feedback loop to continuously promote TNBC malignant behaviors.

Dual-luciferase report assay confirmed that there is a direct interaction between MALAT1 and miR-30c, and Runx2 is a direct target of miR-30c. MALAT1 over-expression promoted VSMCs calcification, which was at least partially through regulating the miR-30c/Runx2 axis.

MALAT1 is overexpressed in HCC, and higher expression is associated with worse prognosis. MALAT1 mRNA level may serve as a prognostic marker for patients with HCC after hepatectomy.

MALAT1 promoted RB cell proliferation and repressed cell apoptosis by repressing miR-598-3p to activate the PI3K/AKT pathway. MALAT1 repressed miR-598-3p to activate the PI3K/AKT pathway, thus facilitating cell proliferation and inhibiting cell apoptosis in RB.

Targeting MALAT1 by CRISPR/Cas9 technique inhibit the cell proliferation and migration, and in addition induce apoptosis. Thus, MALAT1 can act as a tumor biomarker and therapeutic target.

Moreover, CRNDE overexpression attenuated the effects of MALAT1 overexpression. Overall, MALAT1 might form a negative feedback loop with CRNDE in sepsis to regulate lung cell apoptosis.

In comparison with the DEX group, mice in the DEX + MALAT1 group had larger tumors, with the up-regulation of Ki-67 and the down-regulation of active caspase-3. DEX can reduce the expression of MALAT1 in EC cells, thereby inhibiting the proliferation, invasion and migration, as well as EMT, and promoting the apoptosis of EC cells.

Consistent with the results observed in vitro, we also found that the OCa tumor weight and volume of nude mice injected with lncRNA MALAT1 overexpression vector were enhanced and JAK2 protein level increased remarkably in comparison to the ginkgolic acid group. In summary, GA may exert its inhibitory effect on the proliferative and migratory capacities of OCa cells through suppressing the activity of lncRNA MALAT1/JAK2 axis.

We further manifested that miR-216b facilitated the expressions of apoptosis-related markers, but restrained those of EMT-related markers by repressing MALAT1 expression. Moreover, UTMBs-mediated miR-216b M enhanced the expressions of downstream multiple miRNAs of MALAT1, but this tendency was reversed by co-transfection of overexpressed MALAT1 and miR-216b M. Collectively, UTMBs-mediated miR-216b M restrained NSCLC cell growth by modulating the MALAT1-miRNA axis.

Moreover, the gain-of-function assay validated the function of MAT2A in HPV16-positive cervical cancer proliferation. Taken together, our results demonstrated that MALAT1 acts as a competitive endogenous RNA (ceRNA) to regulate MAT2A by sponging miR-485-5p in HPV16-positive cervical cancer, suggesting that MALAT1 may act as a potential therapeutic target for HPV16-positive cervical cancer.

Together, our findings demonstrate how MALAT1 overexpression facilitates an oncogenic function through inhibiting tumor cell apoptosis, combined with increasing tumor cell inflammation, proliferation, and invasion in the EOC tumor microenvironment. MALAT1 is thus a potential diagnostic marker and therapeutic for this malignancy.

This miR-101-3p inhibition blocked MALAT1. These findings suggest that lncRNA MALAT1 is related to BC pathogenesis using the miR101-3p/mTOR/PKM2 pathway and is a potential therapeutic target.

MALAT1 sponges miR-330-5p to activate NF-κB signal pathway in THP-1 macrophages-derived foam cells. This finding may provide a novel biomarker for AS diagnosis.

We propose that lncRNA MALAT1 interacts with miR-124-3p to modulate OS progression by targeting SphK1. Hence, we identified a novel MALAT1/miR-124-3p/SphK1 signaling pathway in the regulation of OS biological behaviors.

Finally, enhanced renal fibrosis and kidney tissue damage were observed in diabetic rats. In conclusion, MALAT1 overexpression may enhance renal fibrosis in diabetic rats and cell damage in HG-induced HK-2 cells via the miR-2355-3p/IL6ST axis, which provides a new perspective of DN treatment.

The results indicated that compared with NG treatment, HG treatment increased MALAT1 expression levels and decreased miR‑141‑3p expression levels in H9C2 cells. Therefore, the present study suggested that lncRNA‑MALAT1 targeted miR‑141‑3p to promote HG‑induced H9C2 cardiomyocyte pyroptosis.

As a consequence of autophagy inhibition, SQSTM1 accumulation promotes NF-κB translocation to elevate IL-6 expression. Overall, these results demonstrated that intercellular interaction between GC cells and fibroblasts was mediated by autophagy inhibition caused by increased MALAT1 that promotes GC progression, providing novel prevention and therapeutic strategies for GC.

Furthermore, rescue assays revealed that the increase of proinflammatory cytokine production (for TNF-α, p = 0.002, p = 0.015; for IL-1β, p < 0.001, p = 0.006; for IL-6, p = 0.002, p < 0.001) and MUC protein levels (for MUC5AC, p = 0.001, p < 0.001; for MUC8, p < 0.001, p = 0.001) induced by MALAT1 overexpression was neutralized by 4-N-&lsqb;2-(4-phenoxyphenyl) ethyl] quinazoline-4, 6-diamine (QNZ) treatment in LPS- or IL-17A-stimulated HMEECs. In conclusion, MALAT1 promotes inflammatory response in LPS- or IL-17A- stimulated HMEECs via the NF-κB signaling pathway, which may provide a potential novel insight for the treatment of OM.

These data demonstrated that H might be developed as a therapeutics of gastric cancer and lncRNA MALAT1/miR-124-3p/EZH2 axis could be a target for intervention.

In conclusion, MALAT1 was enhanced after PNI and it promoted the proliferation and migration of Schwann cells through sponging miR-129-5p to increase BDNF expression and secretion. This study proved that MALAT1 may be a vital regulator in peripheral nerve regeneration.

The MALAT1/miR-30 cascade also modulated spastin-induced microtubule severing, and the MALAT1/miR-30/spastin axis regulated neurite outgrowth in hippocampal neurons. This study suggests a new mechanism governing neurite outgrowth in hippocampal neurons involving MALAT1/miR-30-regulated spastin expression.

Thus, we demonstrated that lncRNA MALAT1 regulates CCDC80 and LPL expression through miR-141-3p/200a-3p.

MALAT1 promoted cell proliferation and inhibited cell apoptosis of RGCs via targeting miR-149-5p in glaucoma in vitro, which might shed light on the mechanism of glaucoma pathogenesis.

MALAT1 overexpression or miR-124 inhibitor led to increased expression of ZEB2. In summary, our study depicts a novel pathway of MALAT1/miR-124/ZEB2 that regulates the progression of glioma and might provide a promising strategy for glioma therapy.