scholarly journals SINE Insertion in 5’ Flanking of IGFBP3 May Associated With Gene Expression and Phenotypic Variations

2021 ◽  
Author(s):  
Xiaoyan Wang ◽  
Yalong An ◽  
Eduard Murani ◽  
Enrico D'alessandro ◽  
Chengling Chi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Genetic Analysis ◽  
Promoter Activity ◽  
Luciferase Activity ◽  
Muscle Thickness ◽  
Longissimus Muscle ◽  
Activity Assay ◽  
Recombinant Vector ◽  
Luciferase Activity Assay ◽  
Sine Insertion

Abstract Background: Insulin-like growth factor binding proteins (IGFBPs), specifically binding to IGF1 and IGF2, play an important role in regulating physiological functions of insulin-like growth factors (IGFs). IGFBPs have been considered important candidate genes for economic traits due to their involvement in physiological processes related to growth and development. However, most of the current studies on genetic markers of IGFBPs have focused on SNPs, and large fragment insertion mutations such as retrotransposons have rarely been considered. In this paper, we screened the porcine IGFBP genes (IGFBP1-8) for retrotransposon insertion polymorphisms (RIPs) using bioinformatics prediction combined with the PCR-based amplification. Furthermore, for two linked RIPs their population distribution and impact on promoter activity and phenotype were further evaluated.Results: Screening of IGFBPs identified RIPs in IGFBP1-5 and IGFBP7. In total twelve predicted RIPs were confirmed by PCR. These RIPs were detected in different breeds with an uneven distribution among them. By linkage genetic analysis and PCR verification, IGFBP3-1-RIP and IGFBP3-2-RIP are completely linked, showing only three genotypes, SINE+/+/LINE-/-, SINE-/-/LINE+/+ and SINE+/-/LINE-/+. The age of 100 kg body weight and longissimus muscle thickness of Large white individuals of SINE+/+/LINE-/-genotype were significantly (P<0.05) higher than those of SINE+/-/LINE+/- genotype and SINE-/-/LINE+/+ genotype. However, the longissimus muscle thickness and corrected backfat thickness of SINE+/+/LINE-/- individuals were significantly (P<0.05) thinner than those of SINE+/+/LINE-/- genotype. The expression of the IGFBP3 gene in liver, leg muscles and backfat of 30-day Sujiang piglets with SINE+/+/LINE-/- genotype were significantly higher (P<0.05) than those with SINE-/-/LINE+/+ genotype by the real-time quantitative polymerase chain reaction (qPCR). Further study was conducted to confirm the effect of SINE and LINE insertion on the promoter activity of IGFBP3. First, the core promoter region of the IGFBP3 gene was identified locating within 482bp upstream of ATG by using the dual-luciferase activity assay. Then SINE and LINE were combined with 482bp fragment to construct a recombinant vector respectively based on the PGL3-Promoter-Enhancer. The recombinant vector was transfected into C2C12, 3T3-L1, and Hela cells. The detection of the dual-luciferase reporter gene revealed that only SINE insertion was significantly increased (P<0.05) promoter activity of the IGFBP3 gene, indicating that the SINE may act as an enhancer to regulate the promoter activity of the IGFBP3 gene. Conclusions: Overall, this study identified 12 RIPs in IGFBP gene clusters, which provided useful markers for genetic analysis of pig populations. Furthermore, based on the dual-luciferase activity assay in cells and association analysis, the linked genetic variations generated by SINE and LINE insertions in 5’ flanking of IGFBP3 may associated with variations of gene expression and phenotype.

SINE Insertion in 5’ Flanking of Porcine IGFBP3 May Associated with Gene Expression and Phenotypic Variations

2021 ◽  
Author(s):  
xiaoyan wang ◽  
Yalong An ◽  
Eduard Murani ◽  
Enrico D'alessandro ◽  
Chengling Chi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Promoter Activity ◽  
Core Promoter ◽  
Muscle Thickness ◽  
Gene Clusters ◽  
Economic Traits ◽  
Large White ◽  
Physiological Processes ◽  
Luciferase Activity Assay ◽  
Sine Insertion

Abstract Background: Insulin-like growth factor binding proteins (IGFBPs) have been considered important candidate genes for economic traits due to their involvement in physiological processes related to growth and development. However, most of the current studies on genetic markers of IGFBPs have focused on SNPs, and large fragment insertion mutations such as retrotransposons have rarely been considered.Results: In total twelve retrotransposon insertion polymorphisms (RIPs) were confirmed using bioinformatics prediction combined with the PCR-based amplification. By linkage genetic analysis, IGFBP3-1-RIP and IGFBP3-2-RIP are completely linked, showing only three genotypes, SINE+/+/LINE-/-, SINE-/-/LINE+/+ and SINE+/-/LINE-/+. The age of 100 kg body weight and longissimus muscle thickness of Large white individuals of SINE+/+/LINE-/-genotype were significantly (P<0.05) higher than those of other two genotypes. However, corrected backfat thickness of SINE+/+/LINE-/- individuals were significantly (P<0.05) thinner than those of SINE+/+/LINE-/- genotype. The expression of the IGFBP3 gene in liver and backfat of 30-day Sujiang piglets with SINE+/+/LINE-/- genotype were significantly higher (P<0.05) than those with SINE-/-/LINE+/+ genotype by qPCR. After the core promoter region of the IGFBP3 gene was identified locating within 482bp upstream of ATG by using the dual-luciferase activity assay, further study was conducted to confirm the effect of SINE of IGFBP3-1-RIP and LINE of IGFBP3-2-RIP on the promoter activity of IGFBP3 based on the PGL3-Promoter-Enhancer. The result revealed that only SINE insertion was significantly increased (P<0.05) promoter activity of the IGFBP3 gene, indicating that the SINE may act as an enhancer to regulate the promoter activity of the IGFBP3 gene.Conclusions: Overall, this study identified 12 RIPs in IGFBP gene clusters. Furthermore, SINE insertions in 5’ flanking of IGFBP3 may associated with variations of gene expression and phenotype.

scholarly journals Familial Mediterranean fever-related miR-197-3p targets IL1R1 gene and modulates inflammation in monocytes and synovial fibroblasts

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yeliz Z. Akkaya-Ulum ◽  
Tayfun Hilmi Akbaba ◽  
Zeynep Tavukcuoglu ◽  
Jae Jin Chae ◽  
Engin Yilmaz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Familial Mediterranean Fever ◽  
Luciferase Activity ◽  
Synovial Fibroblasts ◽  
Activity Assay ◽  
Functional Assays ◽  
Luciferase Activity Assay ◽  
Mediterranean Fever ◽  
Non Coding Rnas ◽  
Inflammatory Effect

AbstractFamilial Mediterranean fever (FMF); is an autosomal recessively inherited autoinflammatory disease caused by the mutations in the Mediterranean Fever (MEFV) gene. Recent studies have shown that epigenetic control mechanisms, particularly non-coding RNAs, may play a role in the pathogenesis of autoinflammation. microRNAs (miRNAs) are small non-coding RNAs that play critical roles in regulating host gene expression at the post-transcriptional level. The phenotypic heterogeneity of FMF disease suggests that FMF may not be a monogenic disease, suggesting that epigenetic factors may affect phenotypic presentation. Here we examined the potential anti-inflammatory effect of miR-197-3p, which is a differentially expressed miRNA in FMF patients, by using inflammation related functional assays. We monitored gene expression levels of important cytokines, as well as performed functional studies on IL-1β secretion, caspase-1 activation, apoptosis assay, and cell migration assay. These experiments were used to evaluate the different stages of inflammation following pre-miR-197 transfection. Anti-miR-197 transfections were performed to test the opposite effect. 3′UTR luciferase activity assay was used for target gene studies. Our results obtained by inflammation-related functional assays demonstrated an anti-inflammatory effect of miR-197-3p in different cell types (synovial fibroblasts, monocytes, macrophages). 3′UTR luciferase activity assay showed that miR-197-3p directly binds to the interleukin-1beta (IL-1β) receptor, type I (IL1R1) gene, which is one of the key molecules of the inflammatory pathways. This study may contribute to understand the role of miR-197-3p in autoinflammation process. Defining the critical miRNAs may guide the medical community in a more personalized medicine in autoinflammatory diseases.

Phospholipase A 2 Metabolites Mediate Endothelin Stimulation of the Human Brain Natriuretic Peptide Promoter

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 721-721
Author(s):  
Quan He
Keyword(s):  
Gene Expression ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Promoter Activity ◽  
Luciferase Activity ◽  
Phospholipase A ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
P450 Monooxygenase ◽  
Stimulation Of

P155 Brain natriuretic peptide (BNP) gene expression accompanies cardiac hypertrophy and heart failure. The vasoconstrictor endothelin-1 (ET)may be involved in the development of these diseases. ET has also been shown to activate phospholipase A 2 (PLA 2 ). Thus we studied whether ET and PLA 2 metabolites regulate BNP gene expression. The hBNP promoter (-1818 to + 100) coupled to a luciferase reporter gene was transferred into neonatal ventricular myocytes (NVM),and luciferase activity was measured as an index of promoter activity. ET (10 -7 M)induced BNP mRNA in NVM as assessed by Northern blot. It also stimulated the hBNP promoter 4-fold vs control, an effect completely inhibited by actinomycin D. To test the involvement of different PLA 2 isoforms, transfected cells were treated with the Ca ++ -independent PLA 2 (iPLA 2 )inhibitor bromoenol lactone (BEL), the cytosolic PLA 2 inhibitor methyl arachidonyl fluorophosphonate, or the secretory PLA 2 inhibitor ONO-RS-082 prior to stimulation with ET. Only the iPLA 2 inhibitor BEL prevented ET-stimulated hBNP promoter activity. The PLA 2 metabolite lysophosphatidic acid (LPA) also activated the hBNP promoter (2.2-fold; n = 3), but lysophosphatidylcholine did not. To test whether arachidonic acid metabolites are involved in ET’s effect, cells were pretreated with either a lipoxygenase (LO), cyclooxygenase, or p450 monooxygenase inhibitor. Only the LO inhibitor baicalein prevented ET stimulation of the hBNP promoter. Finally, we studied the involvement of cis elements in ET-stimulated hBNP promoter activity. Deletion of BNP promoter sequences from -1818 to -408 and from -408 to -40 reduced ET’s effect by 54% and 78%, respectively. Moreover, ET-stimulated luciferase activity was reduced by 53% when the GATA element (at position -85 relative to the start site of transcription) was mutated. These data suggest that: 1) ET activates the hBNP promoter through a transcriptional mechanism; 2) LPA, perhaps generated by a BEL-sensitive iPLA 2 , is involved in ET’s effect; 3) a LO pathway may also mediate ET signaling; and 4) ET regulation of the hBNP promoter targets both distal and proximal cis elements, including GATA.

scholarly journals ZNF139 increases multidrug resistance in gastric cancer cells by inhibiting miR-185

2018 ◽  
Vol 38 (5) ◽  
Author(s):  
Bibo Tan ◽  
Yong Li ◽  
Qun Zhao ◽  
Liqiao Fan ◽  
Dong Wang
Keyword(s):  
Gastric Cancer ◽  
Drug Resistance ◽  
Multidrug Resistance ◽  
Cell Lines ◽  
Zinc Finger Protein ◽  
Luciferase Activity ◽  
Cell Activity ◽  
Expression Level ◽  
Activity Assay ◽  
Luciferase Activity Assay

It has been reported that the expression of zinc finger protein 139 (ZNF139) and microRNA-185 (miR-185) were associated with proliferation, drug resistance of gastric cancer (GC) cells. However, the detailed mechanisms have not been fully investigated. The expression of ZNF139 in both GC tissues and cell lines was tested, then SGC7901/ADR or SGC7901 cells were transfected with ZNF139-siRNA, miR-185 analog, or pcDNA-ZNF139. Cell activity was determined by MTT assay. Real-time PCR and Western blot were utilized to detect ZNF139, miR-185, and multidrug resistance (MDR) related genes including MDR1/P-gp, GST-π, MRP-1, Bcl-2, TS and Bax. ChIP and dual luciferase activity assay were used to investigate regulation between ZNF139 and miR-185. Increased ZNF139 and decreased miR-185 expression were detected in GC tissues and cell lines. Transfection with ZNF139-siRNA into SGC7901/ADR cells markedly increased expression of miR-185, and treating with chemotherapeutic drugs ADR, 5-FU, L-OHP, the survival rate of SGC7901/ADR cells obviously decreased after ZNF139-siRNA transfection. On the other hand, transfection with pcDNA-ZNF139 in GC cell line SGC7901 resulted in an increased expression level of ZNF139 and a decline in the expression level of miR-185, meanwhile drug resistance of GC cells was clearly enhanced to ADR, 5-FU, L-OHP. Dual luciferase activity assay demonstrated that ZNF139 inhibited transcriptional activities of miR-185’s promoter in cells transfected with the reporter plasmid encompassing the upstream promoter region of miR-185 along with pcDNA-ZNF139. Our data reveal that ZNF139 might promote MDR gene MDR1/P-gp, MRP-1 and Bcl-2 by prohibiting miR-185.

scholarly journals miR-101-3p Contributes to α-Synuclein Aggregation in Neural Cells through the miR-101-3p/SKP1/PLK2 Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Min Zhang ◽  
Wei Liu ◽  
Qingan Zhang ◽  
Hongfeng Hu
Keyword(s):  
Substantia Nigra ◽  
Target Gene ◽  
Luciferase Activity ◽  
Substantia Nigra Pars Compacta ◽  
Activity Assay ◽  
Protein Ubiquitination ◽  
Ubiquitination Assay ◽  
Luciferase Activity Assay ◽  
Vitro Protein

Parkinson’s disease (PD) is a neurodegenerative disorder characterized by progressive neuronal loss in different brain regions, including the dopaminergic (DA) neurons of the substantia nigra pars compacta (SNc). The aggregation of α-synuclein (α-Syn) plays an essential role in the progression of PD-related neuron toxicity. In this study, bioinformatic analysis was used to confirm differentially expressed genes between patients with PD and healthy donors. Immunofluorescence was used to study the aggregation of α-Syn. Flow cytometry was used to confirm the apoptosis of neurons. Western blot was used to investigate the underlying mechanism. Coimmunoprecipitation (co-IP) was used to verify the interaction between proteins. Luciferase activity assay was used to confirm the target gene of miRNA. In vitro protein ubiquitination assay was used to ascertain the role of S-phase kinase-associated protein 1 (SKP1) on the ubiquitination processes of polo-like kinase 2 (PLK2). The result indicated that miR-101-3p was overexpressed in the substantia nigra of the postmortem brains of patients with PD. The underlying role was investigated in the SH-SY5Y cell line. The overexpression of α-Syn did not result in toxicity or aggregation. However, the co-overexpression of miR-101-3p and α-Syn promoted aggregation and neuron toxicity. Luciferase activity assay indicated that SKP1 is a target gene of miR-101-3p. The co-IP experiment confirmed that SKP1 could directly interact with PLK2. In vitro protein ubiquitination assay confirmed that SKP1 could promote the ubiquitination and subsequent protein degradation of PLK2. We also observed that the cotransfection of short hairpin RNA that targets PLK2 and α-Syn overexpression plasmid results in the endoplasmic reticulum stress of neurons. Our results collectively provide evidence that miR-101-3p contributes to α-Syn aggregation in neurons through the miR-101-3p/SKP1/PLK2 pathway.

miR-628-5p promotes growth and migration of osteosarcoma by targeting IFI44L

2020 ◽  
Vol 98 (2) ◽  
pp. 99-105 ◽  
Author(s):  
Ju-Yong Wang ◽  
Ju-Qiang Wang ◽  
Shi-Bao Lu
Keyword(s):  
Untranslated Region ◽  
Poor Prognosis ◽  
Luciferase Activity ◽  
Gene Expression Omnibus ◽  
Migration And Invasion ◽  
Activity Assay ◽  
Luciferase Activity Assay ◽  
And Migration ◽  
Geo Database

This study investigated the role of miR-628-5p and interferon-induced protein 44-like (IFI44L) in osteosarcoma (OS) and determined whether miR-628-5p modulated OS growth by regulating IFI44L. Based on the data downloaded from Gene Expression Omnibus (GEO) database, we revealed that the expression of IFI44L was downregulated in OS and low expression of IFI44L was correlated with better prognosis of patients with OS. Biological prediction of its upstream regulatory miRNAs on the miRWalk website found that miR-628-5p is a possible upstream regulatory miRNA of IFI44L. Luciferase activity assay demonstrated that miR-628-5p could bind to the 3′ untranslated region (UTR) of IFI44L, which proved the above prediction. The expression of miR-628-5p is upregulated in OS and high expression of miR-628-5p is correlated with poor prognosis of patients with OS. The results of RT-qPCR showed that the expression of miR-628-5p in MG-63, U2OS, Saos-2, and SW1353 cells was significantly higher than that in the hFOB1.19 cells. Downregulation of miR-628-5p by miR-628-5p inhibitor significantly inhibited the proliferation, migration, and invasion of MG-63 cells. By rescue assay, we found that knockdown of IFI44L rescued the proliferation and motility of miR-628-5p depleted MG-63 cells. Collectively, our present data illustrated that miR-628-5p promoted the growth and motility of OS at least partly by targeting IFI44L. Moreover, miR-628-5p and IFI44L might be proposed as promising biomarkers in OS diagnosis and treatment.

Variants in miRNA regulome and their association with the risk of nonsyndromic orofacial clefts

Epigenomics ◽  
2020 ◽  
Vol 12 (13) ◽  
pp. 1109-1121
Author(s):  
Guirong Zhu ◽  
Chi Zhang ◽  
Yuting Wang ◽  
Yuli Wang ◽  
Dandan Li ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Cleft Lip ◽  
Target Gene ◽  
Luciferase Activity ◽  
Nucleotide Polymorphisms ◽  
Activity Assay ◽  
Orofacial Clefts ◽  
Enhancer Activity ◽  
Single Nucleotide ◽  
Luciferase Activity Assay

Aim: To investigate the associations between single nucleotide polymorphisms (SNPs) in miRNA regulome and nonsyndromic orofacial clefts. Materials & methods: The associations were evaluated by logistic regression model in stage I (504 cases and 455 controls) and stage II (1500 cases and 1386 controls). Functional experiments including luciferase activity assay, cell apoptosis and proliferation, serum miRNA expression, and mouse embryo RNA sequencing were performed. Results: Rs3830766 in the enhancer of hsa-miR-4260 was associated with cleft lip only (CLO) and enhancer activity. Hsa-miR-4260 expression decreased in the serum of CLO. Overexpression of miR-4260 inhibited cell proliferation and promoted cell apoptosis. UBB was the target gene of hsa-miR-4260. Conclusion: Rs3830766 in the hsa-miR-4260 enhancer that can interact with UBB was relevant to CLO.

scholarly journals The tumor-suppressive function of miR-1296-5p by targeting EGFR and CDK6 in gastric cancer

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Yan Jia ◽  
Lian-Mei Zhao ◽  
Han-Yu Bai ◽  
Cong Zhang ◽  
Su-Li Dai ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Target Genes ◽  
Luciferase Activity ◽  
Clinical Stage ◽  
Migration And Invasion ◽  
Cancer Tissue ◽  
Activity Assay ◽  
Luciferase Activity Assay

AbstractWe aimed to confirm the role of miR-1296-5p in gastric cancer and to identify its target genes. The expression of miR-1296-5p was measured in gastric cancer tissues and cell lines. The function of miR-1296-5p was examined by the overexpression and inhibition of its expression in typical gastric cell lines as well as SGC-7901 and MGC-803 cells. The targets of miR-1296-5p were identified by a luciferase activity assay. We found that miR-1296-5p was down-regulated in gastric cancer tissue and cell lines, and low expression levels of miR-1296-5p were associated with advanced clinical stage. Moreover, miR-1296-5p inhibited cell proliferation, migration, and invasion in SGC-7901 and MGC-803 cells. Then, we identified CDK6 and EGFR as novel targets of miR-1296-5p by a luciferase activity assay. Furthermore, the overexpression of miR-1296-5p suppressed the expression of CDK6 and EGFR. Our results indicated a tumor-suppressive role of miR-1296-5p through the translational repression of oncogenic CDK6 and EGFR in gastric cancer.

scholarly journals In vitroAnticancer Activities of Some Triterpene Glycosides from Holothurians of Cucumariidae, Stichopodidae, Psolidae, Holothuriidae and Synaptidae families

2016 ◽  
Vol 11 (9) ◽  
pp. 1934578X1601100 ◽  
Author(s):  
Sergey N. Fedorov ◽  
Sergey A. Dyshlovoy ◽  
Alexandra S. Kuzmich ◽  
Larisa K. Shubina ◽  
Sergey A. Avilov ◽  
...  
Keyword(s):  
Cellular Response ◽  
Antitumor Agents ◽  
Luciferase Activity ◽  
Nuclear Factor Κb ◽  
Soft Agar ◽  
Triterpene Glycosides ◽  
Activator Protein 1 ◽  
Activity Assay ◽  
Luciferase Activity Assay ◽  
Apoptosis And Necrosis

Triterpene glycosides isolated from holothurians are natural products known to possess cytotoxic properties against cancer cells. However, their anticancer prophylactic activity has not been studied sufficiently. The anticancer prophylactic, cytotoxic, and pro-apoptotic properties of 18 triterpene glycosides, as well as their effects on the transcriptional activities of activator protein-1 (AP-1) and nuclear factor-κB (NF-κB), were examined using methods that included EGF-induced JB6 Cl41 P+ cell transforation in soft agar, flow cytometry, MTS assessment of cell viability, and a luciferase activity assay. The compounds inhibited EGF-induced neoplastic JB6 Cl41 P+ cell transforation in soft agar and caused apoptosis and necrosis of human HL-60 and THP-1 leukemia cells. AP-1 and NF-κB were involved in the cellular response to the treatment by the compounds. Conclusion: glycosides isolated from holothurians of Cucumariidae, Stichopodidae, Psolidae, Holothuriidae and Synaptidae families have potential for development as new antitumor agents and as instruments to study AP-1 and NF-κB.

scholarly journals Mitochondrial creatine kinase 1 in non-small cell lung cancer progression and hypoxia adaptation

2021 ◽  
Author(s):  
Ming Li ◽  
Huan Liu ◽  
Jinwen Li ◽  
Shuai Guo ◽  
Yan Lv ◽  
...  
Keyword(s):  
Western Blot ◽  
Luciferase Activity ◽  
Specific Inhibitor ◽  
Activity Assay ◽  
Small Cell Lung ◽  
Mitochondrial Creatine Kinase ◽  
Qrt Pcr ◽  
Hypoxia Adaptation ◽  
Luciferase Activity Assay

Abstract Background Hypoxia is a prominent feature of solid cancer. This research aims to expose the role of mitochondrial creatine kinase 1 (CKMT1) in non-small cell lung cancer (NSCLC) progression and hypoxia adaptation. Methods The mRNA and protein expression of CKMT1 in NSCLC tissues and cells were detected using GEPIA web, immunohistochemistry, qRT-PCR and western blot. Cells were exposed to a hypoxic chamber with atmosphere containing 5% CO2, 1% O2 and residual N2. The protein levels of HIF-1α and CKMT1 in H1650 and H1299 cells exposed to hypoxia were determined by western blot. Luciferase activity assay and HIF1 specific inhibitor (LW6) assay indicated the related function of HIF-1 and CKMT1. The role of CKMT1 to NSCLC cells biological function on hypoxic condition was measured by CCK8, colony formation, transwell and apoptosis assay. Results CKMT1 was highly expressed in NSCLC tissues and cells using GEPIA web, immunohistochemistry, qRT-PCR and western blot. Hypoxia induced the accumulation of HIF-1α and the expression of CKMT1 in H1650 and H1299 cells. The results of luciferase activity assay and HIF1 specific inhibitor (LW6) assay indicated that HIF-1, as a transcription factor of CKMT1, up-regulated the expression of CKMT1 under hypoxic conditions. Further, knockdown of CKMT1 inhibited the cell proliferation and invasion of H1650 and H1299 cells, which could be rescued by hypoxia. Conclusions In summary, CKMT1 has the potential as a target for NSCLC hypoxic targeted therapy.

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