MiR-4303 relieves chondrocyte inflammation by targeting ASPN in osteoarthritis

Abstract Background Osteoarthritis (OA) is a severe articular cartilage disease whose pathogenesis involves the inflammation of chondrocytes. MicroRNAs (miRNAs) are considered to be effective inflammation regulators. However, the regulatory mechanism of miRNAs in osteoarthritis needs to be further elucidated. In this paper, we aim to investigate the underlying mechanisms by which miR-4303 regulates osteoarthritis. Methods RT-qPCR is performed to detect the levels of miR-4303, ASPN, PDIA3, PIK3CA, and TRAF3; CCK-8 assay is conducted to evaluate chondrocyte viability; EdU assay was carried to assess chondrocyte proliferation; western blot is conducted to measure the levels of ASPN, PCNA, Ki-67, CyclinA1, CyclinB1, CyclinD2, p27, Bax, Bcl-2, cleaved caspase-3, and Cleaved caspase-9 proteins; FACs is performed to detect the distribution of chondrocytes in each cell cycle and chondrocyte apoptosis; ELISA is conducted to assess the levels of TNF-β, IL-1β and IL-6 in the supernatant of chondrocytes; the potential binding sites of miR-4303 and ASPN are predicted by miRDB software, which is confirmed by the dual-luciferase reporter gene assay. Results Our findings illustrated that miR-4303 was down-regulated in arthritic tissues and LPS-induced chondrocytes; miR-4303 overexpression rescued LPS-induced chondrocyte viability, proliferation and cell cycle and alleviated LPS-induced chondrocyte apoptosis; miR-4303 overexpression inhibited the release of inflammatory factors in LPS-induced chondrocytes; miR-4303 targeted ASPN and miR-4303 relieved chondrocyte inflammation via targeting ASPN. Conclusion MiR-4303 serves as a prognostic biomarker and relieves chondrocyte inflammation via targeting ASPN. Our findings provide novel prognostic biomarkers in predicting the progression and prognosis of osteoarthritis.

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MiR-4303 relieves chondrocyte inflammation by targeting ASPN in osteoarthritis

Journal of Orthopaedic Surgery and Research ◽

10.1186/s13018-021-02731-9 ◽

2021 ◽

Vol 16 (1) ◽

Author(s):

Chunyu Wang ◽

Li Wang ◽

Xingfa Guan ◽

Changfeng Yue

Keyword(s):

Cell Cycle ◽

Inflammatory Factors ◽

Luciferase Reporter ◽

Luciferase Reporter Gene ◽

Ki 67 ◽

Chondrocyte Viability ◽

Expression Levels ◽

Gene Assay ◽

Underlying Mechanisms ◽

Cartilage Disease

Abstract Background Osteoarthritis (OA) is a severe articular cartilage disease whose pathogenesis involves the inflammation of chondrocytes. MicroRNAs (miRNAs) are considered to be effective inflammation regulators. However, the regulatory mechanism of miRNAs in osteoarthritis needs to be further elucidated. In this paper, we aim to investigate the underlying mechanisms by which miR-4303 regulates osteoarthritis. Methods RT-qPCR is performed to detect the mRNA expression levels of miR-4303, ASPN, PDIA3, PIK3CA, and TRAF3. CCK-8 assay and EdU assay are carried to assess chondrocyte viability. The protein expression levels of ASPN, PCNA, Ki-67, CyclinA1, CyclinB1, CyclinD2, p27, Bax, Bcl-2, cleaved caspase-3, and Cleaved caspase-9 were measured by western blot. FACs is performed to detect the cell cycle and apoptosis of chondrocyte. ELISA is conducted to assess the levels of TNF-β, IL-1β and IL-6 in the supernatant of chondrocytes. The potential binding sites of miR-4303 and ASPN are predicted by the miRDB database and confirmed by the dual-luciferase reporter gene assay. Results Our findings illustrated that miR-4303 was down-regulated in arthritic tissues and LPS-induced chondrocytes; miR-4303 overexpression rescued the decrease in cell viability, cell cycle arrest and apoptosis induced by LPS. Furthermore, miR-4303 overexpression inhibited the release of inflammatory factors in LPS-induced chondrocytes, miR-4303 relieved chondrocyte inflammation via targeting ASPN. Conclusion MiR-4303 serves as a prognostic biomarker and relieves chondrocyte inflammation via targeting ASPN. Our findings provide novel prognostic biomarkers in predicting the progression and prognosis of osteoarthritis.

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Overexpressed miR-375-Loaded Restrains Development of Cervical Cancer Through Down-Regulation of Frizzled Class Receptor 4 (FZD4) with Liposome Nanoparticle as a Carrier

Journal of Biomedical Nanotechnology ◽

10.1166/jbn.2021.3145 ◽

2021 ◽

Vol 17 (9) ◽

pp. 1882-1889

Author(s):

Suqin Wang ◽

Lina Xu ◽

Zhiqiang Zhang ◽

Ping Wang ◽

Rong Zhang ◽

...

Keyword(s):

Cell Cycle ◽

Cervical Cancer ◽

Cell Proliferation ◽

Protein Expression ◽

Signaling Pathway ◽

Luciferase Reporter ◽

Luciferase Reporter Gene ◽

Gene Assay ◽

M Phase ◽

The Impact

Dysregulation expression of miR-375 is noted to correlate with progression of cervical cancer. This study attempted to investigate the impact of overexpressed miR-375-loaded liposome nanoparticles on proliferation of cervical cancer (CC), to provide an insight on pathogenesis of CC disorder. CC cells were co-cultured with pure liposome nanoparticles (empty vector group), miR-375 agonist-loaded liposome nanoparticles, or transfected with miR-375 antagonist. Besides, some cells were exposed to TGF-β/Smads signaling pathway inhibitor or activator whilst cell proliferation was assessed by MTT assay, and expressions of FZD4 and miR-375 were determined. Western blot analysis was carried out to detect the expression of TGF-β pathway factors (TGF-β, Smad2, Smad7, p-Smad2) and its downstream Smads pathway. The interaction between miR-375 and FZD4 was evaluated by dual-luciferase reporter gene assay. Overexpression of miR-375 induced arrest at the G0/G1 phase of cell cycle and elevation of Smad2 protein expression (P <0.05), with lower expressions of TGF-β, Smad7, p-Smad2, and FZD4, while transfection with miR-375 inhibitor exhibited opposite activity. Presence of miR-375 agonist-loaded liposome nanoparticles induced decreased cell proliferation. There was a targeting relationship between miR-375 and FZD4, and administration with TGF-β/Smads agonist resulted in increased miR-375 and Smad2 expressions, as well as decreased TGF-β, Smad7, p-Smad2, FZD4 protein expression, and the number of S phase and G2/M phase cells (P < 0.05). The signaling inhibitor oppositely suppressed cell proliferation decreasing miR-375 expression. miR-375-loaded liposome nanoparticles activated TGF-β/Smads signaling pathway to restrain cell cycle and suppress cell division, and proliferation through targeting FZD4 in CC. Its molecular mechanism is related to activation of TGF-β/Smads signaling pathway.

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MicroRNA-137-mediated inhibition of lysine-specific demethylase-1 prevents against rheumatoid arthritis in an association with the REST/mTOR axis

Molecular Pain ◽

10.1177/17448069211041847 ◽

2021 ◽

Vol 17 ◽

pp. 174480692110418

Author(s):

Wei Sun ◽

Yijun Zhang ◽

Guanghui Wang

Keyword(s):

Rheumatoid Arthritis ◽

Mtor Pathway ◽

Cell Counting ◽

Inflammatory Factors ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Luciferase Reporter Gene ◽

Lysine Specific Demethylase ◽

Gene Assay

Background It has been increasingly reported that microRNAs (miRNAs) are related to rheumatoid arthritis (RA) pathogenesis. This present research was conducted to analyze the functions of miR-137 and the underlying molecular mechanism in RA progression. Methods Differentially expressed miRNAs in RA patients were analyzed using microarray-based analyses. Next, experiments involving miR-137 overexpression were performed to analyze the role of miR-137 in human fibroblast-like synoviocytes-RA (HFLS-RA) using cell counting kit-8 (CCK-8) assay, EdU staining, Transwell assay and flow cytometry, respectively. The function of miR-137 in inflammation was determined using ELISA. The binding relationship between miR-137 and LSD1 was confirmed by dual-luciferase reporter gene assay and ChIP test. Besides, a rat model with RA was established for in vivo experiments. Results miR-137 was downregulated in RA tissues and cells, which was negatively correlated with inflammatory factors. Upregulated miR-137 suppressed growth, migration and invasion of HFLS-RA, but promoted apoptosis. Lysine-specific demethylase-1 (LSD1) was a target of miR-137 and could be negatively regulated by miR-137. Moreover, LSD1 could activate REST through demethylation, while the REST/mTOR pathway induced levels of pro-inflammatory factors in RA. We observed the similar results in our in vivo study. Conclusion This study suggested that miR-137 reduced LSD1 expression to inhibit the activation of REST/mTOR pathway, thus preventing against inflammation and ameliorating RA development. Our research may offer new insights into treatment of RA.

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miRNA-576 Alleviates the Malignant Progression of Atherosclerosis through Downregulating KLF5

Disease Markers ◽

10.1155/2021/5450685 ◽

2021 ◽

Vol 2021 ◽

pp. 1-8

Author(s):

Jing Wang ◽

Lihui Zhang ◽

Ting Wang ◽

Caige Li ◽

Lijing Jiao ◽

...

Keyword(s):

Body Weight ◽

Caspase 3 ◽

Malignant Progression ◽

Raw264.7 Cells ◽

Inflammatory Factors ◽

Luciferase Reporter ◽

Inflammatory Factor ◽

Luciferase Reporter Gene ◽

Gene Assay

Objective. To elucidate the role of microRNA-576 (miRNA-576) in alleviating the deterioration of atherosclerosis (AS) through downregulating krüpple-like factor 5 (KLF5). Materials and Methods. The AS model in mice was first constructed. Body weight, inflammation degrees, blood lipid, and relative levels of KLF5, miRNA-576, caspase-3, and bcl-2 in AS mice and control mice were compared. Dual-luciferase reporter gene assay was performed to evaluate the binding between miRNA-576 and KLF5. RAW264.7 cells were treated with 200 mg/L ox-LDL for establishing in vitro high-fat model. Regulatory effects of miRNA-576/KLF5 on relative levels of β-catenin and inflammatory factors in RAW264.7 cells were explored. Results. Body weight was heavier in AS mice than in controls. Protein levels of KLF5 and caspase-3 were upregulated, while bcl-2 was downregulated in AS mice. In particular, protein level of KLF5 was highly expressed in aortic tissues of AS mice. TC and LDL increased, and HDL decreased in AS mice compared with controls. Inflammatory factor levels were markedly elevated in AS mice. KLF5 was verified to be the target gene binding miRNA-576. Overexpression of miRNA-576 downregulated KLF5, inflammatory factors, and β-catenin in ox-LDL-treated RAW264.7 cells. Regulatory effect of miRNA-576 on the release of inflammatory factors in RAW264.7 cells could be partially abolished by KLF5. Conclusions. miRNA-576 alleviates malignant progression of AS via downregulating KLF5.

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Circular RNA CCDC66 Regulates Osteoarthritis Progression by Targeting miR-3622b-5p

Gerontology ◽

10.1159/000520325 ◽

2022 ◽

pp. 1-11

Author(s):

Chengyuan Zhang ◽

Ye Lu ◽

Feng Yuan ◽

Shilin Jiang

Keyword(s):

Reporter Gene ◽

Bioinformatics Analysis ◽

Reporter Gene Assay ◽

Luciferase Reporter ◽

Chondrocyte Apoptosis ◽

Luciferase Reporter Gene ◽

Luciferase Reporter Gene Assay ◽

Tnf Α ◽

Gene Assay ◽

Sirt3 Expression

Objective: CircCCDC66 is involved in cancer progression, but its role in osteoarthritis (OA) remains unknown. This study was carried out to explore the biological role of circCCDC66 in OA and its underlying mechanism. Methods: The expression levels of miR-3622b-5p and circCCDC66 in OA cartilage tissues were detected by qRT-PCR. Cell Counting Kit-8 (CCK8) and flow cytometry were used to detect the chondrocyte viability and apoptosis. The expression of chondrocyte inflammatory factors (IL-6 and TNF-α) was measured by ELISA. The target genes of circCCDC66 and miR-3622b-5p were analyzed by bioinformatics analysis and luciferase reporter gene assay. The relationship between circCCDC66 and miR-3622b-5p was analyzed by bioinformatics analysis and luciferase reporter gene assay. Results: It was found that circCCDC66 expression in OA cartilage tissues was upregulated. CircCCDC66 overexpression inhibited proliferation and promoted apoptosis of chondrocytes and increased IL-6 and TNF-α levels in chondrocytes. miR-3622b-5p was predicted to be a downstream target gene of circCCDC66, and circCCDC66 overexpression inhibited miR-3622b-5p expression in chondrocytes. Moreover, miR-3622b-5p expression was downregulated in OA cartilage tissues. miR-3622b-5p overexpression increased chondrocyte proliferation, inhibited chondrocyte apoptosis, and enhanced the expression of IL-6 and TNF-α in chondrocytes. In addition, circCCDC66 overexpression enhanced SIRT3 expression in chondrocytes, while miR-3622b-5p overexpression inhibited SIRT3 expression in chondrocytes. Conclusion: CircCCDC66 promoted OA chondrocyte apoptosis by regulating the miR-3622b-5p/SIRT3 axis. CircCCDC66 may be a new therapeutic target of OA.

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miR-636 Inhibits EMT, Cell Proliferation and Cell Cycle of Ovarian Cancer by Directly Targeting the Transcription Factor Gli2 of Hedgehog Pathway

10.21203/rs.3.rs-52894/v1 ◽

2020 ◽

Author(s):

Jiong Ma ◽

Chunxia Zhou ◽

Xuejun Chen

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Protein Expression ◽

Luciferase Reporter ◽

Luciferase Reporter Gene ◽

Cell Proliferation And Migration ◽

Gene Assay ◽

And Migration ◽

Proliferation And Migration

Abstract Objective: Ovarian cancer (OVC) is the fifth leading cause of cancer-related deaths in women and has a significant impact on physical and mental health of women. This study explores the molecular mechanism of miR-636 acting as a tumor suppressor in OVC in vitro and in vivo, and provides new insight into the treatment of OVC.Methods: Protein-protein interaction (PPI) analysis was performed to identify the hub gene in Hedgehog (Hh) pathway. TargetScan database was used to predict the upstream regulatory miRNAs of Gli2 to obtain the target miRNA. qRT-PCR was performed to test the expression of miR-636, while Western blot were conducted to detect the expression of Hh and EMT (epithelial-mesenchymal transition) related genes in OVC cell lines. MTT assay and wound healing assay were used to measure the effect of miR-636 on OVC cell proliferation and migration. Flow cytometry was carried out to examine the effect of miR-636 on cell cycle, and Western blot was used for identification of changes in expression of Hh and EMT related proteins. Dual-luciferase reporter gene assay was implemented to detect the targeted relationship between miR-636 and Gli2. The xenotransplantation model was used to detect the effect of miR-636 on OVC cell proliferation in vivo.Results: PPI interaction analysis found that Gli2 was the hub gene in Hh pathway. Based on TargetScan and GEO databases, Gli2 was found to be targeted regulated by the upstream miR-636. In vitro experiments discovered that miR-636 was significantly lowly expressed in OVC cell lines. Overexpressing miR-636 significantly inhibited HO-8910PM cell proliferation and migration abilities as well as induced cell cycle arrest in G0/G1 phase, while the inhibition of miR-636 promoted cell proliferation and migration abilities. Dual-luciferase reporter gene assay revealed that Gli2 was a target gene of miR-636. Besides, overexpressing miR-636 decreased protein expression of Gli2, while the inhibition of miR-636 increased protein expression of Gli2. Furthermore, the overexpression and inhibition of miR-636 both affected the expression of proteins related to Hh signaling pathway and EMT. Rescue experiments verified that overexpression of Gli2 reversed the inhibitory effect of miR-636 on HO-8910PM cell proliferation and migration abilities, and attenuated the blocking effect of miR-636 on HO-8910PM cell cycle. The xenotransplantation model suggested that miR-636 inhibited cell growth of OVC by decreasing Gli2 expression. Besides, overexpressing Gli2 potentiated the EMT process in OVC via decreasing E-cadherin protein expression and increasing Vimentin protein expression, and it reversed the inhibitory effect of miR-636 on OVC cell proliferation and migration abilities in vivo.Conclusion: miR-636 inhibits the Hh pathway activation via targeted binding to Gli2, thus inhibiting EMT, cell proliferation and migration in OVC.

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Mir10a overexpression aggravates the renal ischemia-reperfusion injury associated with a decrease in PIK3CA

10.21203/rs.2.23453/v2 ◽

2020 ◽

Author(s):

Dongsheng Xu ◽

Wenjun Li ◽

Tao Zhang ◽

Gang Wang

Keyword(s):

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Luciferase Reporter ◽

Akt Pathway ◽

Luciferase Reporter Gene ◽

Gene Assay ◽

Underlying Mechanisms ◽

Related Proteins ◽

Hypoxia Reoxygenation

Abstract Background: To investigate the effect of miR-10a on the renal tissues with ischemia-reperfusion (I/R) injury in rats and explore the underlying mechanisms of miR-10a in the HK-2 cells of hypoxia-reoxygenation. Methods: The miR-10a level was measured in renal tissues with I/R rats by RT-PCR. In order to research the role of miR-10a in the renal tissues, miR-10 agonist and miR-10a antagonist were used to treat I/R rats. The levels of serum creatinine (Scr) and blood urea nitrogen (BUN) in serum, renal histopathology, apoptosis of cells in renal tissues were analyzed, separately. The phosphatidylinositol 3-kinase (PI3K)/Akt pathway related proteins were measured by Western blot. The HK-2 cell was cultured to study the mechanism of miR-10a in the model of hypoxia-reoxygenation. The dual luciferase reporter gene assay was used to confirm the PI3K p100 catalytic subunit α (PIK3CA) was a target gene of miR-10a. Results: After renal I/R injury in rats, the miR-10a expression was significantly increased (p<0.05). Injection of miR-10a agonist significantly aggravated the injury of renal and raised the apoptosis of cells in renal in rats with renal I/R injury (p<0.05). However, administration of miR-10a antagonist obviously improved the injury of renal, decreased the renal cells apoptosis and inhibited the PI3K/Akt pathway activity (p<0.05). In vitro experiments, the negative relation between PIK3CA and miR-10a was confirmed. Further, overexpression of miR-10a significantly decreased the proliferation of HK-2 cells, and increased the cells apoptosis via up-regulating PI3K/Akt pathway (p<0.05). Conclusion: miR-10a could aggravate the renal I/R injury associated with a decrease in PIK3CA/PI3K/Akt pathway.

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Human Umbilical Cord Mesenchymal Stem Cells-Derived Exosomal MicroRNA-18b-3p Inhibits the Occurrence of Preeclampsia by Targeting LEP

Nanoscale Research Letters ◽

10.1186/s11671-021-03475-5 ◽

2021 ◽

Vol 16 (1) ◽

Author(s):

Qin Huang ◽

Meng Gong ◽

Tuantuan Tan ◽

Yunong Lin ◽

Yan Bao ◽

...

Keyword(s):

Stem Cells ◽

Mesenchymal Stem Cells ◽

Umbilical Cord ◽

Serum Levels ◽

Inflammatory Factors ◽

Luciferase Reporter ◽

Human Umbilical Cord ◽

Luciferase Reporter Gene ◽

Fetal Rat ◽

Gene Assay

AbstractExosomes derived from human umbilical cord mesenchymal stem cells (hucMSCs) expressing microRNAs have been highlighted in human diseases. However, the detailed molecular mechanism of hucMSCs-derived exosomal miR-18b-3p on preeclampsia (PE) remains further investigation. We aimed to investigate the effect of exosomes and miR-18b-3p/leptin (LEP) on occurrence of PE. The morphology of the hucMSC and hucMSC-exosomes (Exos) was identified. The exosomes were infected with different lentivirus expressing miR-18b-3p to explore the role of miR-18b-3p in PE. The PE rat model was established by intraperitoneal injection of N-nitro-l-arginine methyl ester. The expression of LEP and miR-18b-3p was tested in PE rat placenta tissues. Also, the effect of exosomes on LEP and miR-18b-3p expression was detected. The systolic blood pressure (SBP), proteinuria, inflammatory factors, the weight of fetal rat and placenta and cell apoptosis in PE rats were detected. Finally, the relationship between miR-18b-3p and LEP was verified using dual-luciferase reporter gene assay and RNA pull-down assay. Exosomes, restoring miR-18b-3p or inhibiting LEP reduced SBP and proteinuria of PE rats as well as increased the weight of fetal rat and placenta, decreased serum levels of inflammatory factors as well as suppressed apoptotic cells of PE rats, exerting a suppressive effect on PE progression. miR-18b-3p was decreased and LEP was increased in placenta tissues of PE rats. LEP was the direct target gene of miR-18b-3p. Upregulation of miR-18b-3p or treatment of the exosomes suppressed LEP expression and reduced PE occurrence, while downregulation of miR-18b-3p had contrary effects. Downregulated LEP reversed the effect of miR-18b-3p reduction on PE rats. HucMSCs-derived exosomal miR-18b-3p targets LEP to participate in the occurrence and development of PE. This study may provide a novel theoretical basis for the mechanism and investigation of PE.

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Tanshinone IIA Attenuates Inflammatory Responses by Downregulating MicroRNA-23b, Upregulating TRIB1 and Inactivation of the TLR4/NF-κB Signaling Pathway in THP-1 Macrophages

10.21203/rs.3.rs-23071/v1 ◽

2020 ◽

Author(s):

Wei Ji ◽

Gengyao Li ◽

Yuqian Liu ◽

Xiaofeng Yan

Keyword(s):

Signaling Pathway ◽

Inflammatory Responses ◽

Drug Effect ◽

Tanshinone Iia ◽

Inflammatory Factors ◽

Luciferase Reporter ◽

Inflammatory Factor ◽

Luciferase Reporter Gene ◽

Migration Ability ◽

Gene Assay

Abstract Background: Atherosclerosis is a kind of chronic cardiovascular disease, and Tanshinone IIA (Tan) is a naturally derived anti-inflammatory compound. In this study, we aim to explore the biological role of Tan and regulatory mechanism in atherosclerosis.Methods: Firstly, the model of atherosclerosis mice was constructed. The area of atherosclerosis, the level of blood lipid and the content of inflammatory factors were measured in mice treated with Tan. After that, the differentially expressed microRNAs (miRNAs) were obtained by microarray analysis of mice plasma. The effect of miR-23b on cell migration ability, adhesion ability and inflammatory factor level of macrophages treated with Tan. After that, we determined the target mRNA of miR-23b through the bioinformatics analysis and the dual luciferase reporter gene assay. THP-1 macrophages were treated with miR-23b mimic or si-TRIB1 to detect the activity of the TLR4/NF-κB signaling pathway via immunohistochemistry.Results: Tan injection significantly improved atherosclerosis inflammation in mice, especially in mice treated with 90 mg/kg dose. miR-23b was obtained by differential screening, which can significantly inhibit the drug effect of Tan, and aggravate the occurrence of atherosclerosis. miR-23b targeted TRIB1, the decrease of TRIB1 also inhibited the drug effect of Tan. The up regulation of miR-23b enhanced the activity of TLR4/NF-κB pathway, and TLR4/NF-κB pathway inhibited the drug effect of Tan on the inflammatory response.Conclusion: Overall, Tan could protect macrophage against inflammation via inactivating TLR4/NF-κB pathway by down-regulating miR-23b and upregulating TRIB1, providing a novel theoretical foundation for treatment of atherosclerosis.

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miR-301b-3p promotes lung adenocarcinoma cell proliferation, migration and invasion by targeting DLC1

10.21203/rs.3.rs-27752/v1 ◽

2020 ◽

Author(s):

Haitao Liu ◽

Xingjie Ma ◽

Niu Niu ◽

Junjie Zhao ◽

Chao Lu ◽

...

Keyword(s):

Cell Proliferation ◽

Lung Adenocarcinoma ◽

Molecular Mechanisms ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Luciferase Reporter Gene ◽

Promoting Effect ◽

Luciferase Reporter Gene Assay ◽

Gene Assay ◽

Underlying Mechanisms

Abstract Background miR-301b-3p has been reported to be abnormally expressed in various human cancers including lung cancer. However, the underlying role and molecular mechanisms in lung adenocarcinoma (LUAD) remain unclear. This study aimed to elucidate the underlying mechanisms of miR-301b-3p in LUAD. Methods Based on TCGA database, we found that miR-301b-3p was prominently up-regulated in LUAD tissues. A series of functional experiments including CCK-8 assay, colony formation assay and Transwell assay uncovered that the up-regulation of miR-301b-3p facilitated LUAD cell proliferation, migration and invasion abilities. Bioinformatics analysis and dual-luciferase reporter gene assay demonstrated that Deleted in Liver Cancer 1 (DLC1) was negatively regulated by miR-301b-3p, and it was extremely lowly expressed in LUAD tissues and cells. Results Rescue experiments suggested that overexpressing DLC1 restored the promoting effect of miR-301b-3p on LUAD cell proliferation, migration and invasion. Conclusions Taken together, our study elucidated that miR-301b-3p promoted LUAD cell proliferation, migration and invasion by targeted suppressing DLC1 expression. The discovery of the mechanism provides a novel therapeutic strategy for LUAD patients, which helps to improve the survival of patients.

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