Silencing of miR490–3p by H. pylori activates DARPP-32 and induces resistance to gefitinib

Zhu, Shoumin; Khalafi, Shayan; Chen, Zheng; Poveda, Julio; Peng, Dunfa; Lu, Heng; Soutto, Mohammed; Que, Jianwen; García-Buitrago, Mónica; Zaika, Alexander; El–Rifai, Wael

doi:10.1016/j.canlet.2020.07.014

Cited by 10 publications

(8 citation statements)

References 42 publications

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“…Correlation analyses revealed a negative correlation between miR‐490‐3p and ELOA (Figure 7B). Furthermore, recent studies reported that miR‐490‐3p expression is reduced in GC and associated with poor prognosis 18,19 . These results encouraged us to hypothesize that increased expression of ELOA might be attributed to decreased miR‐490‐3p abundance in GC.…”

Section: Resultsmentioning

confidence: 90%

“…Furthermore, recent studies reported that miR-490-3p expression is reduced in GC and associated with poor prognosis. 18,19 These results encouraged us to hypothesize that increased expression of ELOA might be attributed to decreased miR-490-3p abundance in GC. Luciferase assays confirmed the regulation of ELOA by miR-490-3p both in both HEK293T and AGS suggesting that ELOA is a direct target of miR-490-3p (Figure 7C-E).…”

Section: Eloa Is a Novel Target Of Mir-490-3pmentioning

confidence: 95%

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ELOA promotes tumor growth and metastasis by activating RBP1 in gastric cancer

Tian,

Gong,

Hao

et al. 2023

Cancer Medicine

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BackgroundElongin A (ELOA), our previous work revealed, serves as a novel tumor suppressor in colorectal cancer. However, the function and mechanism of ELOA in other cancer types, including gastric cancer (GC), remain to be elucidated.MethodsThe expression of ELOA was measured by quantitative reverse transcription‐polymerase chain reaction and western blot. The effects of ELOA on GC growth and metastasis were assessed through a series of in‐vitro and in‐vivo assays. Furthermore, the potential mechanism of ELOA was revealed by RNA sequencing, dual luciferase reporter assay, chromatin immunoprecipitation, and rescue experiments in GC.ResultsWe uncovered increased expression of ELOA in GC tissues compared with paired normal tissues via bioinformatic analyses and our sample detection. Enhanced ELOA expression in GC tissues was obviously correlated with poor tumor differentiation, lymph node metastasis, advanced tumor stage, and a poor prognosis. A series of functional experiments showed that ELOA promoted the proliferation and metastasis of GC. Mechanistically, we revealed that the decreased levels of miR‐490‐3p caused the upregulation of ELOA in GC. Both RNA‐seq and ChIP assays revealed that ELOA transcriptionally activated retinol‐binding protein 1 (RBP1) by binding to its promotor. Furthermore, specific knockdown of RBP1 reduced the tumor‐promoting ability of ELOA in GC cells.ConclusionsIn summary, our findings demonstrate that ELOA exerts oncogenic properties by activating RBP1 expression, providing the basis for a promising therapeutic target in GC.

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Section: Resultsmentioning

confidence: 90%

Section: Eloa Is a Novel Target Of Mir-490-3pmentioning

confidence: 95%

ELOA promotes tumor growth and metastasis by activating RBP1 in gastric cancer

Tian,

Gong,

Hao

et al. 2023

Cancer Medicine

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“…At the highest concentration tested (50 µg/ml), both AGN-Pure and AC2 significantly reduced the viability of the A549 cells compared to the control group (0 µg/ml), indicating AGN was effective against lung cancer. AGN acts as an antiprofilating agent by activating the apoptosis pathway that decreases the PI3K/Akt signaling, triggering cancer cell death and preventing lung tumor [18], [46]. Half maximal inhibitory concentration (IC50) was also calculated, indicating the concentration of a flavonoid (AGN) and product AC2 SDSD needed to inhibit the growth of cancer cells by 50%.…”

Section: Anti-proliferative Activitymentioning

confidence: 99%

Development and Characterization of Chitosan-Based Spray-Dried Solid Dispersions of Apigenin: 3D Printed Shell-Pill for Improved Efficacy of Model Flavonoid

Alali¹,

Ahmed²,

Fatima³

et al. 2023

Preprint

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This study aimed to develop chitosan-based apigenin spray dried solid dispersion using 1:1,1:1.5,1:2 w/w ratios. The results of process yield and drug assay were found to be (87.5%, 94.2%, and 95.86%), (95.2 ±1.34%), (99.5 ±0.85%), and (97.6 ±2.42%), respectively, for AC1, AC2, and AC3. Flow properties indicate the free flow of powders. FTIR revealed compatibility among chitosan and apigenin, and DSC and XRD showed prepared solid dispersion was on a molecular level and available in amorphous. In contrast, SEM images reflect irregular block and near-spherical shape elongated particles in the selected AC2. The antimicrobial examination reflects that AC2 was more effective against Gram-positive, negative, and fungal strains. AC2 SDSDs has more anti-oxidant property compared to pure flavonoid (AGN). Anti-proliferative activity against A549 lung cancer cell lines showed better anti-cancer activity by AC2 SDSDs. The selected AC2 SDSD filled in a 3D shell pill and further characterized for 3D shell pill for dissolution profiles and stability studies. The product has sustained release and similar release profiles after three months of storage. The findings suggest that the AC2 SDSDs may be a promising candidate for further development as a 3D printed drug delivery system for treating multiple disease conditions using model flavonoid- apigenin.

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“…Hypermethylation-mediated silencing of miR-490-3p reactivates SWI/SNF-related, matrixassociated, actin-dependent regulator of chromatin, subfamily d, member 1 (SMARCD1), a chromatin remodeling complex subunit, to impart a malignant phenotype of GC cells [85]. Furthermore, down-regulation of miR490-3p also promotes gefitinib resistance by inducing activation of DARPP-32/PI3K/Akt and STAT3 signaling pathways [86]. Inhibition of miR-210 expression enhances cell proliferation by activating its target stathmin 1 (STMN1) and dimethyladenosine transferase 1 (DIMT1) [87].…”

Section: Helicobacter Pylori-induced Gastric Cancermentioning

confidence: 99%

Crosstalk between Environmental Inflammatory Stimuli and Non-Coding RNA in Cancer Occurrence and Development

Xie

Jing

et al. 2021

Cancers

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There is a clear relationship between inflammatory response and different stages of tumor development. Common inflammation-related carcinogens include viruses, bacteria, and environmental mutagens, such as air pollutants, toxic metals, and ultraviolet light. The expression pattern of ncRNA changes in a variety of disease conditions, including inflammation and cancer. Non-coding RNAs (ncRNAs) have a causative role in enhancing inflammatory stimulation and evading immune responses, which are particularly important in persistent pathogen infection and inflammation-to-cancer transformation. In this review, we investigated the mechanism of ncRNA expression imbalance in inflammation-related cancers. A better understanding of the function of inflammation-associated ncRNAs may help to reveal the potential of ncRNAs as a new therapeutic strategy.

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Silencing of miR490–3p by H. pylori activates DARPP-32 and induces resistance to gefitinib

Cited by 10 publications

References 42 publications

ELOA promotes tumor growth and metastasis by activating RBP1 in gastric cancer

ELOA promotes tumor growth and metastasis by activating RBP1 in gastric cancer

Development and Characterization of Chitosan-Based Spray-Dried Solid Dispersions of Apigenin: 3D Printed Shell-Pill for Improved Efficacy of Model Flavonoid

Crosstalk between Environmental Inflammatory Stimuli and Non-Coding RNA in Cancer Occurrence and Development

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