Circulating miR-320a Acts as a Tumor Suppressor and Prognostic Factor in Non-small Cell Lung Cancer

Khandelwal, Akanksha; Sharma, Uttam; Barwal, Tushar Singh; Seam, Rajeev Kumar; Gupta, Manish; Rana, Manjit Kaur; Vásquez, Karen M.; Jain, Aklank

doi:10.3389/fonc.2021.645475

Cited by 34 publications

(26 citation statements)

References 56 publications

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“…Both miR-181a-5p [43,44] and miR-320a [45] target AKT3, a key regulator of the PI3K-AKT-mTOR signaling pathway, a pathway that is known to be dysregulated in ASD and is a potential therapeutic target in ASD [46]. miR-320a has been shown to promote myocardial fibroblast proliferation by regulating the PIK3CA/Akt/mTOR signaling pathway in HEH2 cells [47].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Expression Profiles in Autism Spectrum Disorder: Role for miR-181 in Immunomodulation

Frye

Rose

McCullough

et al. 2021

JPM

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Background: MicroRNAs (miRNAs) are important regulators of molecular pathways in psychiatric disease. Here, we examine differential miRNAs expression in lymphoblastoid cell lines (LCLs) derived from 10 individuals with autism spectrum disorder (ASD) and compare them to seven typically developing unrelated age- and gender-matched controls and 10 typically developing siblings. Small RNAseq analysis identified miRNAs, and selected miRNAs were validated using quantitative real-time polymerase reaction (qRT-PCR). KEGG analysis identified target pathways, and selected predicted mRNAs were validated using qRT-PCR. Results: Small RNAseq analysis identified that multiple miRNAs differentiated ASD from unrelated controls and ASD from typically developing siblings, with only one, hsa-miR-451a_R-1, being in common. Verification with qRT-PCR showed that miR-320a differentiated ASD from both sibling and unrelated controls and that several members of the miR-181 family differentiated ASD from unrelated controls. Differential expression of AKT2, AKT3, TNF α and CamKinase II predicted by KEGG analysis was verified by qRT-PCR. Expression of CamKinase II βwas found to be correlated with the severity of stereotyped behavior of the ASD participants. Conclusions: This study provides insight into the mechanisms regulating molecular pathways in individuals with ASD and identifies differentiated regulated genes involved in both the central nervous system and the immune system.

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Section: Discussionmentioning

confidence: 99%

MicroRNA Expression Profiles in Autism Spectrum Disorder: Role for miR-181 in Immunomodulation

Frye

Rose

McCullough

et al. 2021

JPM

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“…When the cells were at approximately 80% confluence, si-ATG2B, si-negative control (NC), mimic negative control (NC), miR-320a mimic, inhibitor negative control (NC), and miR-320a inhibitor were transiently transfected into the tumor cells using Lipofectamine 2000, following the manufacturer’s guidelines. After a 48 h incubation in 37°C and 5% CO 2 , the transfected tumor cells were used for further assays [ 17 ].…”

Section: Methodsmentioning

confidence: 99%

“…The mutant reporter vector pMIR-GLO- ATG2B -MUT was obtained by a site-directed mutagenesis kit (New England Biolabs). A431 and SCL-1 cells were co-transfected with miR-320a mimics or scramble control and with pMIR-GLO- ATG2B-WT or MUT reporter vector using Lipofectamine 2000 (Thermo Fisher Scientific) and incubated for 48 h. luciferase activities were then assessed with the Dual-Luciferase Reporter Assay System (Promega) [ 17 ]. All experiments were plated in triplicate and repeated thrice.…”

Section: Methodsmentioning

confidence: 99%

Crocin exerts anti-proliferative and apoptotic effects on cutaneous squamous cell carcinoma via miR-320a/ATG2B

Jiang

Luan

et al. 2021

Bioengineered

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Cutaneous squamous cell carcinoma (cSCC) is a highly prevalent skin malignancy, and the effective therapy still remains a challenge. Crocin can be used for cSCC therapy. This study explored the effects of cSCC cells treatment with crocin in vitro and in vivo. The study used A431 and SCL-1 cells lines, cSCC human samples and BALB/C nude mice for investigations. Apoptosis was determined by MTT assays, while miR-320a and ATG2B expressions were validated through RT-qPCR. Interaction of miR-320a with ATG2B was examined via dual luciferase reporter assay. The autophagy and apoptosis proteins expressions were further confirmed through western blot and immunofluorescence staining assays. The results indicated a significantly upregulated miR-320a, but a down-regulated ATG2B expression in the cSCC clinical samples. Crocin significantly repressed cSCC cells growth, and induced apoptosis through autophagy. Furthermore, miR-320a expression was inhibited and ATG2B expression was increased. Dual luciferase reporter assay revealed that miR-320a regulated ATG2B expression directly. Additionally, the upregulation of ATG2B expression in cSCC cells inhibited cell proliferation and led to cell apoptosis. Crocin also reduced tumor growth and stimulated the apoptosis in vivo. In conclusion, miR-320a is upregulated and ATG2B is down-regulated in cSCC, Crocin suppresses the proliferation and induces apoptosis of cSCC cells. Further, Crocin increases autophagy while miR-320a hinders autophagy and the apoptotic effects of crocin on cSCC cells. MiR-320a binds ATG2B directly, and ATG2B expression is upregulated by crocin. Finally, Crocin triggers cSCC cells apoptosis in vivo. Crocin can target ATG2B/miR-320a and may be an effective alternative for cSCC treatment.

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“…Lipofectamine 3000 (Invitrogen, USA) was employed as the transfection reagent and the transfection was performed based on manufacturer’s protocols. After an incubation of 48 h in 37°C and 5% CO2, the transfected cells were used for subsequent assays [ 22 ].…”

Section: Methodsmentioning

confidence: 99%

“…The mutant reporter vector pMIR-GLO- FOXO1 -MUT was made by a site-directed mutagenesis kit (New England Biolabs). Hep-2 and Tu177 cells were co-transfected with miR-26a mimics or scramble control and with pMIR-GLO- FOXO1-WT or MUT reporter vector through the use of Lipofectamine 2000 (Thermo Fisher Scientific) and incubated for 48 h. Luciferase activities were then determined using the Dual-Luciferase Reporter Assay System (Promega) [ 22 ]. All the assays were repeated thrice and plated in triplicates.…”

Section: Methodsmentioning

confidence: 99%

Sevoflurane promotes the apoptosis of laryngeal squamous cell carcinoma in-vitro and inhibits its malignant progression via miR-26a/FOXO1 axis

et al. 2021

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Laryngeal squamous cell carcinoma (LSCC) is a laryngeal malignancy with a high mortality rates, and its treatment remains difficult. Sevoflurane is a surgical anesthesia which has anti-tumor effect. This investigation assessed the effects of LSCC cells treatment with Sevoflurane in vitro and in vivo. Hep-2 and Tu177 cells, human LSCC samples and BALB/C nude mice were used for result assessments. Cell viability, proliferation, migration and invasion were assessed via Cell Count Kit-8, wound healing assay and transwell invasion assay respectively. MiR-26a and FOXO1 expressions was examined by qRT-PCR. FOXO1, E-cadherin, N-cadherin and vimentin activities were examined by Western blotting. Moreover, animal experiments were performed to verify our findings in vitro. Lastly, miR-26a and FOXO1 expression levels in clinical samples were analyzed. According to the results, Sevoflurane decreased LSCC cells' viability and even stimulated their apoptosis in vitro and in vivo. Moreover, it could reduce the migration, invasion and EMT. Mechanistically, sevoflurane could downregulate miR-26a expression and that miR-26a could negatively modulate FOXO1 activity. Thus, sevoflurane could increase FOXO1 activity. In the clinical samples, miR-26a expression was significantly upregulated, but FOXO1 was remarkably down-regulated and miR-26a expression in LSCC was linked with better prognosis. In conclusion, MiR-26a is increased and FOXO1 is reduced in human LSCC, Sevoflurane inhibits proliferation and mediates apoptosis of LSCC cells. Further, MiR-26a binds FOXO1 directly, and FOXO1 expression is down-regulated by Sevoflurane. Finally, Sevoflurane triggers LSCC cells apoptosis in vivo. Sevoflurane use to target miR-26a/FOXO1 may be a novel alternative for LSCC therapy.

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Circulating miR-320a Acts as a Tumor Suppressor and Prognostic Factor in Non-small Cell Lung Cancer

Cited by 34 publications

References 56 publications

MicroRNA Expression Profiles in Autism Spectrum Disorder: Role for miR-181 in Immunomodulation

MicroRNA Expression Profiles in Autism Spectrum Disorder: Role for miR-181 in Immunomodulation

Crocin exerts anti-proliferative and apoptotic effects on cutaneous squamous cell carcinoma via miR-320a/ATG2B

Sevoflurane promotes the apoptosis of laryngeal squamous cell carcinoma in-vitro and inhibits its malignant progression via miR-26a/FOXO1 axis

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