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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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At least 1,171 records · Page 65
All sourcesNASA NTRSDOE OSTI
DOE OSTI2018

Upregulation of CDCA5 promotes gastric cancer malignant progression via influencing cyclin E1

Highlights: • Upregulation of CDCA5 correlates with more advanced clinical features and worse survival in gastric cancer patients. • Inhibition of CDCA5 suppresses gastric cancer cells proliferation in vitro and tumor growth in vivo. • CDCA5 promotes gastric cancer malignant progression via influencing cyclin E1 expression. The cell division cycle associated 5(CDCA5) was reported to be associated with progression of several human cancers, however, its clinical significance and biological role still remain unknown in gastric cancer(GC). By analyzing The Cancer Genome Atlas(TCGA), we found CDCA5 was significantly upregulated in GC tissues compared to adjacent normal tissues. Tissue microarray(TMA) indicated upregulation of CDCA5 was significantly correlated with more advanced clinicopathological features, and acts as an independent risk factor for worse overall survival(OS) in GC patients. Moreover, silence of CDCA5 suppresses proliferation of GC cells by inducing G1-phase arrest via downregulating Cyclin E1(CCNE1). Our results demonstrate upregulation of CDCA5 promotes GC malignant progression, which may offer a potential prognostic and therapeutic strategy.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

PMN inhibits colorectal cancer cells through inducing mitotic arrest and p53-dependent apoptosis via the inhibition of tubulin polymerization

Highlights: • PMN inhibits CRC cell proliferation through inducing mitotic arrest and apoptosis. • PMN induces mitotic arrest via the inhibition of microtubule polymerization. • PMN-induced mitotic arrest results in apoptosis and p53 upregulation. • PMN-induced apoptosis is partially mediated by p53. Colorectal cancer (CRC) is the third most prevalent malignancy worldwide. New understandings about this disease are urgently required to guide clinical therapies. In this study, we focused on the effects of the small molecule PMN on CRC cells. PMN dose-dependently inhibited CRC cell proliferation through inducing mitotic arrest and apoptosis. PMN induced mitotic arrest via the disruption of spindle apparatus by inhibiting microtubule polymerization. PMN-induced mitotic arrest resulted in apoptosis and p53 upregulation. Furthermore, p53 upregulation sensitized PMN-induced mitotic cells to apoptosis. This study deepens the understanding of the effects of p53 on the response of CRC cells to PMN, providing the basis for the potential development of PMN as a lead compound of microtubule-destabilizers for p53-positive CRC treatment.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

PPM1B depletion in U2OS cells supresses cell growth through RB1-E2F1 pathway and stimulates bleomycin-induced cell death

Highlights: • PPM1B depletion causes growth suppression in U2OS cells. • PPM1B depletion causes RB1 phosphorylation. • PM1B depletion up-regulates E2F1 target genes in a p38 dependent manner. • PPM1B depletion stimulates bleomycin-induced cell death. PPM1B is a metal-dependent serine/threonine protein phosphatase, with a similar structure and function to the well-known oncogene in breast cancer, PPM1D (WIP1). However, clinical significance of PPM1B as a pharmacological target in cancer therapy has not been explored. To test if PPM1B can be a drug target in the cellular proliferation and death pathway, the lentiviral PPM1B shRNA was stably expressed in cancer cell lines and its regulatory function in the RB1-E2F1 pathway was examined. We found that PPM1B depletion suppressed cellular proliferation of U2OS cells, accompanied by hyper-phosphorylation of RB1 and up-regulation of E2F1 target genes, p27 and caspase 7. Notably, PPM1B depletion significantly sensitised U2OS cells to bleomycin-induced cell death at a minimal effective concentration. Our results suggest that PPM1B plays a negative role in the activation of the p38-RB1-E2F1 pathway and that targeting PPM1B could be useful in certain types of cancer by stimulating chemotherapy-induced cell death.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Silencing LncRNA LOXL1-AS1 attenuates mesenchymal characteristics of glioblastoma via NF-κB pathway

Highlights: • LncRNA LOXL1-AS1 expression is increased in mesenchymal subtype of GBM. • Knocking down LOXL1-AS1 could suppresse GBM cell proliferation. • Silencing LncRNA LOXL1-AS1 Attenuates Mesenchymal Characteristics of Glioblastoma via reducing NF-κB transcription activity. The mesenchymal (MES) subtype of glioblastoma (GBM) suggested worse prognosis and a more malignant phenotype in comparison with their proneural (PN) counterpart. The plasticity between PN and MES transcriptome signatures provided clinical intervention with an manner. Few LncRNA, however, have been discovered to take part in the shift between subtypes. Here, we used transcriptomic data and experimental evidences to demonstrate that silencing LncRNA LOXL1-AS1 was a new regulator of NF-κB signaling pathway through repressing RELB directly, resulting in increased marker genes of PN subtype and decreased those of MES.GBM cell proliferation was functionally suppressed by LOXL1-AS1's knockdown expression,. Furthermore, RELB's rescue could reverse LOXL1-AS1's effects partially in GBM malignant behaviors. LOXL1-AS1 could clinically serve as a poor prognostic indicator for GBM patients. In conclusion, our results suggest that LOXL1-AS1 contributes to aggressive biological processes that are related with MES phenotype via NF-κB signaling, which expand our perceptions into the underlying mechanisms in LOXL1-AS1-based and subtype transition adapted medicine for GBM management.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Identifying the SUMO1 modification of FAM122A leading to the degradation of PP2A-Cα by ubiquitin-proteasome system

Highlights: • FAM122A can be modified by SUMO1 and the sumoylation is desumoylated by SENP1. • The SUMO1 modification site of FAM122A is lysine 89. • The sumoylated FAM122A degrades PP2A-Cα protein by ubiquitin-proteasome system. • The sumoylated FAM122A reduces the activity of PP2A and suppresses cell proliferations. FAM122A is a highly conserved protein in mammals. Here, we identify that FAM122A can be sumoylated at lysine 89, which can be de-conjugated by SENP1. Furthermore, the sumoylation of FAM122A reduces the PP2A-Cα protein level together with the reduced phosphatase activity of PP2A, which suppresses cell proliferation. Collectively, our results suggest that the sumoylation of FAM122A may have a significant role in cellular function.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

ShRNA-mediated knock-down of CXCL8 inhibits tumor growth in colorectal liver metastasis

Highlights: • Showed an up regulation of chemokines (1, 2, 3, 5 and 8) in the tumor invasion front compared to inner parts of the tumor in a xenograft model of colorectal liver metastasis. • Upregulation of CXCL8 in the invasion front of tumor cells is able to promote colorectal liver metastasis. • ShRNA mediated knockdown of CXCL8 in LS174T cells resulted in significantly decreased cell proliferation, migration and invasion in vitro and in a near complete reduction of tumor growth in vivo. • Results suggest an association between CXCL8 expression and progression of colorectal carcinoma and the development of colorectal liver metastases. • CXCL8 may serve as a potential therapeutic target for the treatment of colorectal liver metastasis. CXCL8 belongs to proinflammatory chemokines that are predominantly involved in neutrophil chemotaxis and degranulation. Several studies have suggested that secretion of CXCL8 from cancer cells have a profound effect on tumor microenvironment. In this study, in continuation to our previous work of understanding the global picture of invasion related genes in colorectal liver metastases, we clearly show an up-regulation of CXCL8 expression in the tumor cells at the invasion front as compared to the tumor cells in the inner parts of the tumor. Furthermore, ShRNA mediated down-regulation of CXCL8 resulted in inhibition of cell proliferation, viability and invasion in vitro and a near complete growth reduction of tumor in vivo. We showed that CXCL8 secreted by tumor cells at the invasion front were able to promote migration through angiogenesis by upregulating VEGFA and invasion via the AKT/GSK3β/β-catenin/MMP7 pathway by upregulating BCL-2 confirming the key role of CXCL8 during tumor progression.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Mutual suppression of miR-125a and Lin28b in human hepatocellular carcinoma cells

MicroRNA-125a exhibits an antiproliferative activity and is downregulated in several types of tumors, including hepatocellular carcinoma where it targets sirtuin-7, matrix metalloproteinase-11, and c-Raf. Another target of miR-125a is Lin28, a pluripotency factor that is generally undetectable in differentiated cells but is often upregulated/reactivated in tumors where it acts as an oncogenic factor promoting cell proliferation and tumor progression. In this study we show that downregulation of Lin28b by miR-125a partially accounts for its antiproliferative activity toward hepatocellular carcinoma cells. We also found that Lin28b is able to bind a conserved GGAG motif of pre-miR-125a and to inhibit its maturation in hepatocellular carcinoma cells. Reciprocal inhibition between miR-125a and Lin28b reasonably generates a positive feedback loop where reactivation of Lin-28b inhibits the expression of both miR-125a and let-7, reinforcing its own expression and leading to a marked overexpression of the mitogenic targets of the two miRNAs. On the other hand, perturbation of these circuits by overexpression of miR-125a suppresses Lin28b leading to a decreased cell proliferation. Overall, these data support a tumor suppressive role for miR-125a and contribute to the elucidation of its molecular targets.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Circular RNA hsa{sub c}ircRNA{sub 1}03809 promotes lung cancer progression via facilitating ZNF121-dependent MYC expression by sequestering miR-4302

Lung cancer characterized with malignant cell growth is the leading cause of cancer-related deaths. In recent years, several circular RNAs (circRNAs) have been reported to participate in lung cancer progression. However, the correlation between circular RNA (circRNA) and lung cancer still remains to be further investigated. In this study, we screened out a highly expressed circular RNA hsa{sub c}ircRNA{sub 1}03809 in lung cancer tissues. We showed hsa{sub c}ircRNA{sub 1}03809 could serve as a prognostic biomarker for patients with lung cancer. Furthermore, we found that hsa{sub c}ircRNA{sub 1}03809 knockdown significantly suppressed lung cancer cell proliferation and invasion in vitro and delayed tumor growth in vivo. In mechanism, we identified hsa{sub c}ircRNA{sub 1}03809 as a sponge of miR-4302 targeting ZNF121. By sequestering miR-4302, hsa{sub c}ircRNA{sub 1}03809 promoted the expression of ZNF121 which consequently enhanced MYC protein level in lung cancer cells. Through rescue assays, we demonstrated hsa{sub c}ircRNA{sub 1}03809 contributed to lung cancer cell proliferation and invasion via facilitating ZNF121-dependent MYC expression by sponging miR-4302. In conclusion, our findings illustrated a novel hsa{sub c}ircRNA{sub 1}03809/miR-4302/ZNF121/MYC regulatory signaling pathway in lung cancer progression.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

circRNA{sub 0}084043 promote malignant melanoma progression via miR-153-3p/Snail axis

Highlights: • circRNA{sub 0}084043 was significantly up-regulated in melanoma tissue. • circRNA{sub 0}084043 promotes melanoma cell proliferation, invasion and migration. • circRNA{sub 0}084043 directly binds to miR-153-3p, and Snail is directly targeted by miR-153-3p. • circRNA{sub 0}084043 act as the sponge of miR-153-3p to up-regulate Snail expression, and consequently function as an oncogene in melanoma. Circular RNAs (circRNAs) has been found to play an important role in the regulation of multiple diseases, and participate in cancer development. However, the role of circRNA in malignant melanoma has not been reported. In this study, human circRNA microarray was used to screen the dysregulated circRNA in melanoma. We found that circRNA{sub 0}084043 was significantly up-regulated in melanoma tissue, and the result was replicated in a larger sample size. High circRNA{sub 0}084043 expression was an independent risk factor of overall survival in melanoma patients. circRNA{sub 0}084043 promotes melanoma cell proliferation, invasion and migration. Bioinformatics and luciferase reporter assays confirmed that circRNA{sub 0}084043 directly binds to miR-153-3p, and Snail is directly targeted by miR-153-3p. We also demonstrated that circRNA{sub 0}084043 may act as the sponge of miR-153-3p to up-regulate Snail expression, and consequently function as an oncogene in melanoma. Overall, this result elucidates a new mechanism for circRNA{sub 0}084043 in melanoma development and provides a potential therapeutic target for melanoma patients.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

The long non-coding RNA PCSEAT exhibits an oncogenic property in prostate cancer and functions as a competing endogenous RNA that associates with EZH2

Highlights: • PCSEAT is specifically overexpressed in prostate cancer. • PCSEAT promotes the growth and motility of prostate cancer cells. • PCSEAT regulates EZH2 by competitively ‘sponge’ miRNA-143-3p and miRNA-24-2-5p. • PCSEAT may serve as a biomarker for EZH2 inhibitors. • PCSEAT can be transmitted via exosomes and function in recipient cell. Prostate cancer (PCa) is the most common malignancy and the leading cause of cancer deaths in males. Recent studies demonstrate that long non-coding RNAs (lncRNAs) are involved in many aspects of PCa. However, their biological roles in PCa remain imperfectly understood. Here, we characterized an lncRNA, PCa specific expression and EZH2-associated transcript (PCSEAT, annotated as PRCAT38), which is specifically overexpressed in PCa. We further demonstrated that knockdown of PCSEAT results in the reduction of PCa cell growth and motility, and overexpression of PCSEAT reverses these phenotypes. Furthermore, bioactive PCSEAT is incorporated into exosomes and transmitted to adjacent cells, thus promoting cell proliferation and motility. Mechanistically, we found that PCSEAT promotes cell proliferation, at least in part by affecting miR-143-3p- and miR-24-2-5p-mediated regulation of EZH2, suggesting that PCSEAT and EZH2 competitively ‘sponge’ miR-143-3p and miR-24-2-5p. Overall, our results reveal that PCSEAT is specifically overexpressed in PCa patients and a potential oncogene in PCa cells via mediating EZH2 activity, indicating that PCSEAT may be a potential therapeutic target in PCa.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Inhibition of TBK1 reduces choroidal neovascularization in vitro and in vivo

Highlights: • The expression of TBK1 and VEGF is up-regulated in CNV model. • Knockdown of TBK1 alleviates CNV formation via inhibiting VEGF expression. • TBK1 plays a critical role in the development of CNV. choroidal neovascularization (CNV), a characteristic of wet age-related macular degeneration (AMD), causes severe vision loss among elderly patients. TANK-binding kinase 1 (TBK1) is a ubiquitously expressed serine–threonine kinase and is found to induce endothelial cells proliferation, represent a novel mediator of tumor angiogenesis and exert pro-inflammatory effect. However, the role of TBK1 in choroidal neovascularization has not been investigated so far. In this study, we found that the expression of TBK1 and VEGF was up-regulated in RF/6 A cells chemical hypoxia model and laser-induced mouse CNV model. Silencing of TBK1 suppressed the proliferation and tube formation activity of RF/6 A cells. Intravitreal injection of anti-TBK1 monoclonal antibody ameliorates CNV formation. Taken together, these findings exhibit a proangiogenic role for TBK1 via upregulating the expression of VEGF, and may suggest that TBK1 inhibition offers a unique and alternative method for prevention and treatment of AMD.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

UBE2S enhances the ubiquitination of p53 and exerts oncogenic activities in hepatocellular carcinoma

Highlights: • High expression of UBE2S is significantly correlated with poor outcomes in two independent cohorts containing 845 patients. • UBE2S promotes cell proliferation and migration in HCC. • UBE2S exerts oncogenic activities via enhancing the ubiquitination of p53. Ubiquitin-conjugating enzyme E2S (UBE2S) plays pivotal roles in the progression of human cancers. However, its clinical significance and role in hepatocellular carcinoma (HCC) remain unknown. Here, we show that UBE2S is upregulated in HCC and exhibits oncogenic activities via enhancing the ubiquitination of p53. Increased expression of UBE2S was significantly correlated with higher serum AFP level, higher pathological grade, advanced TNM stage, larger tumor size, vascular invasion and unfavorable patient survivals in two independent cohorts containing a total of 845 patients with HCC. Multivariate analyses by cox regression model suggested UBE2S as an independent factor for overall survival. In vitro experiments demonstrated that UBE2S overexpression promoted, whereas UBE2S knockdown suppressed cell proliferation and migration via modulation of p53 signaling pathway. Ectopic expression of UBE2S upregulated the expression of p53 and its downstream effectors, such as p21 and Cyclin D1. Mechanistically, UBE2S enhanced the ubiquitination of p53 protein to facilitate its degradation in HCC cells. Re-expression of p53 partially attenuated the UBE2S-promoted malignant phenotypes. Collectively, our study provides compelling evidence that UBE2S is a potential prognostic factor and functions as an oncogene in HCC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

The anti-tumor effect of regorafenib in lung squamous cell carcinoma in vitro

Highlights: • Regorafenib might be a potential therapeutic medicine for LSCC treatment. • GSK3β activation restricted the anti-tumor activity of regorafenib on LSCC. • GSK3β inhibition could sensitize the anti-proliferation effect of regorafenib. Lung squamous cell carcinoma (LSCC) is a common type of non-small-cell lung cancer (NSCLC) and lacks effective treatment. Regorafenib, an oral multikinase inhibitor, has demonstrated promising anti-tumor activity in various solid tumors. To study whether regorafenib inhibits LSCC cells, we investigate the compound in several LSCC cell lines and explore the possible mechanism. In this study, we confirmed that regorafenib had anti-proliferation effect on LSCC cell lines by inducing G0/G1 arrest. In addition, glycogen synthase kinase 3β (GSK3β) remained at the same level and Ser9 phosphorylation of GSK3β decreased with increasing incubation time and increasing regorafenib concentration in LSCC cells. GSK3β inhibition enhanced the anti-tumor activity of regorafenib. Thus, GSK3β activation restricted the anti-cancer effect of regorafenib on LSCC. In conclusion, regorafenib might be a promising drug for LSCC therapy. GSK3β might be a potential target to increase the anti-tumor effect of regorafenib in LSCC cells.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Long non-coding RNA KCNQ1OT1 modulates oxaliplatin resistance in hepatocellular carcinoma through miR-7-5p/ ABCC1 axis

Highlights: • KCNQ1OT1 was significantly up-regulated in oxaliplatin-resistant HCC cells. • Knockdown of KCNQ1OT1 inhibited the cell proliferation, migration, invasion. • KCNQ1OT1 modulated oxaliplatin resistance in HCC through miR-7-5p/ ABCC1 axis. The underlying functions of long non-coding RNAs (lncRNAs) on chemoresistance in multiple cancers have been testified. However, the function and mechanism of lncRNAs on chemoresistance in hepatocellular carcinoma are still confused. In this study, we concentrated on the function and mechanism of KCNQ1OT1 on oxaliplatin resistance in hepatocellular carcinoma. Results showed that KCNQ1OT1 was significantly up-regulated in oxaliplatin-resistant HepG2 and Huh7 cells. Moreover, knockdown of KCNQ1OT1 inhibited the cell proliferation, migration, invasion and reduced the expression of drug-resistant gene (MRP5, MDR1, LRP1). Additionally, bioinformatics analysis and dual-luciferase reporter assay showed that miR-7-5p directly targeted the 3′-UTR of miR-7-5p and ABCC1 mRNA, indicating that KCNQ1OT1 regulated the expression of ABCC1 via endogenous sponging miR-7-5p. Conclusively, KCNQ1OT1 modulated oxaliplatin resistance in hepatocellular carcinoma through miR-7-5p/ABCC1 axis, indicating a novel approach for the treatment of hepatocellular carcinoma.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

DNA copy number gain-mediated lncRNA LINC01061 upregulation predicts poor prognosis and promotes papillary thyroid cancer progression

Several DNA copy number amplifications (CNAs) have been reported in papillary thyroid cancer (PTC). However, the functional role of CNAs in PTC remains very unclear. And whether there is a correlation between long noncoding RNA (lncRNA) and CNA requires to be explored. Here, we identified a novel lncRNA LINC01061. The genomic copy number of LINC01061 is amplified, which leads to its elevated expression level in PTC tissues. Moreover, increased level of LINC01061 was correlated with aggressive clinicopathological characteristics. Functional study indicated that LINC01061 silence significantly inhibited the proliferation, cell-cycle and invasion of PTC cells in vitro and tumor growth in vivo. Mechanistically, we showed that LINC01061 interacted with miR-4316 to promote E2F6 expression. The expression of miR-4316 was downregulated in PTC tissues while that of E2F6 was upregulated. Through rescue assay, we demonstrated that LINC01061 promoted PTC cell proliferation, cell-cycle progression and invasion by regulating miR-4316/E2F6 signaling pathway. In conclusion, our research indicated that LINC01061 might be a target for PTC therapy.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

The FGF2 aptamer inhibits the growth of FGF2-FGFR pathway driven lung cancer cells

Cancers, including lung cancer, are a leading cause of death worldwide. To overcome this deadly disease, multiple modality inhibitors have been developed. These include cytotoxic agents, molecular targeted small molecules, such as tyrosine kinase inhibitors, and neutralizing antibodies. An aptamer is a short single-stranded nucleic acid molecule that is selected in vitro from a large random sequence library based on its high and specific affinity to a target molecule. Aptamers can be applied to therapeutics of various types of diseases, including cancer, due to their strong and specific neutralizing activities. However, the efficacy of aptamer-based therapy for cancer cells is not well characterized. In this study, we aimed to show that the FGF2 aptamer is effective for the treatment of FGF2 dependent lung cancer cells. We previously developed PC9GR lung cancer cells, whose proliferation is dependent on EGFR and FGF2-FGFR pathways in a cell autonomous manner. Using PC9GR cells, we demonstrate that the addition of the FGF2 aptamer induces more significant inhibition of PC9GR cell proliferation than does the addition of EGFR inhibitor alone. Furthermore, the addition of the FGF2 aptamer more significantly inhibits the downstream signals and induces apoptosis to a higher extent than does the addition of EGFR inhibitor alone. Our results show that the FGF2 aptamer inhibits the growth of FGF2-FGFR pathway-dependent lung cancer cells. The findings provide preclinical evidence that aptamers can be useful for cancer treatment.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Decreased expression of protein tyrosine kinase 6 contributes to tumor progression and metastasis in laryngeal squamous cell carcinoma

Highlights: • Overexpression of PTK6 significantly decreased cell growth, clonogenicity, invasion and migration capacity in LSCC. • PTK6 suppresses LSCC proliferation mainly by inhibiting c-myc and cyclinD1 expression. • PTK6 promotes cell apoptosis in LSCC. • PTK6 mitigated LSCC invasion and migration through regulating EMT and MMP-9. PTK6 is involved in cell proliferation, invasion and migration. Patients with lower PTK6 expression predicts poor prognosis of LSCC. However, the mechanism of PTK6 in LSCC progression remains unclear. We investigated the role of PTK6 in the pathogenesis of LSCC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

miR-5590-3p inhibited tumor growth in gastric cancer by targeting DDX5/AKT/m-TOR pathway

Recent evidence suggests that microRNAs play important roles in the negative post-transcriptional regulators with altered expression levels found in gastric cancer (GC). Therefore, we employed explore the anti-cancer miRNA and the potential mechanisms by which miRNAs modulate GC progression. We have predicted GC miRNA expression data sets in TargetScan. miR-5590-3p is higher in adjacent nonmalignant tissue than in cancer tissue in 42 pairs of GC tissues. Functional assays, CCK-8 and colony formation assay, were used to determine the Anti-cancer role of miR-5590-3p in human GC progression. In addition, Ago2-based RIP and dual-luciferase reporter assay were conducted to study the miR-5590-3p as a direct target of DDX5. Next, Xenograft nude mouse models were used to determine the role of miR-5590-3p in GC tumorigenicity in vivo. Upregulation of miR-5590-3p suppressed GC cell proliferation, whereas downregulation of miR-5590-3p promoted GC proliferation in vitro. Furthermore, we identified DDX5 as a direct target of miR-5590-3p, and that the biological function of miR-5590-3p during GC progression in vitro and in vivo is through the DDX5/AKT/m-TOR pathway and downstream cyclinD1 and CDK2 expression. Finally, we confirmed the effect of miR-5590-3p directly targeting DDX5 on the development of gastric cancer through salvage experiments in vivo and in vitro.

60 APPLIED LIFE SCIENCES↗