Characterization of the Bombyx mori Cecropin A 1 promoter regulated by IMD pathway

Cecropin A1 （CeeA1） promoter from Bombyx mori was cloned and character- ized to provide insight into the transcriptional control of this antimicrobial peptide gene upon immune challenges. Reporter gene assays demonstrated that both Escherichia coli and lipopolysaccharide could induce expression in BmE cells but B. bombyseptieus or peptidoglycan failed, and the induction pattern of the reporter gene was coincident with the endogenous CecAl. Analysis of deletion and mutation constructs revealed that the regulatory region was the κB motif located between -176 and -166, and no other pre- dicted elements on CecAl promoter affected its inducibility. Insertion of additional κB motifs increased the activity of CecAl promoter. Furthermore, binding of Relish to lob motif was confirmed by electrophoretic mobility shift assay. These findings indicate the regulatory mechanism of CecAl expression in IMD pathway and suggest an approach of engineering antimicrobial peptide promoter with enhanced activities that may lead to broad applications.

Transcriptome analysis of CD4^(+)T cells from HIV-infected individuals receiving ART with LLV revealed novel transcription factors regulating HIV-1 promoter activity

Some HIV-infected individuals receiving ART develop low-level viremia(LLV),with a plasma viral load of 50-1000 copies/mL.Persistent low-level viremia is associated with subsequent virologic failure.The peripheral blood CD4^(+)T cell pool is a source of LLV.However,the intrinsic characteristics of CD4^(+)T cells in LLV which may contribute to low-level viremia are largely unknown.We analyzed the transcriptome profiling of peripheral blood CD4^(+)T cells from healthy controls(HC)and HIV-infected patients receiving ART with either virologic sup-pression(VS)or LLV.To identify pathways potentially responding to increasing viral loads from HC to VS and to LLV,KEGG pathways of differentially expressed genes(DEGs)were acquired by comparing VS with HC(VS-HC group)and LLV with VS(LLV-VS group),and overlapped pathways were analyzed.Characterization of DEGs in key overlapping pathways showed that CD4^(+)T cells in LLV expressed higher levels of Th1 signature transcription factors(TBX21),toll-like receptors(TLR-4,-6,-7 and-8),anti-HIV entry chemokines(CCL3 and CCL4),and anti-IL-1βfactors(ILRN and IL1R2)compared to VS.Our results also indicated activation of the NF-κB and TNF signaling pathways that could promote HIV-1 transcription.Finally,we evaluated the effects of 4 and 17 tran-scription factors that were upregulated in the VS-HC and LLV-VS groups,respectively,on HIV-1 promoter activity.Functional studies revealed that CXXC5 significantly increased,while SOX5 markedly suppressed HIV-1 tran-scription.In summary,we found that CD4^(+)T cells in LLV displayed a distinct mRNA profiling compared to that in VS,which promoted HIV-1 replication and r+eactivation of viral latency and may eventually contribute to virologic failure in patients with persistent LLV.CXXC5 and SOX5 may serve as targets for the development of latency-reversing agents.

Constructing and Analyzing Fusion Promoter of Partial Sericin 1 and Bombyx A3 Cytoplasmic Actin

Previous report showed that the 209 bp DNA sequence upstream of the sericin 1 transcriptional start site （-586 to -378 bp） is involved in promoting transcription and responsible for the tissue specificity of sericin 1 promoter in silkworm Bombyx mori. In the present study, this 209 bp sequence exhibited enhancive effect by assembling in two different locations of ubiquitous Bombyx A3 cytoplasmic actin promoter. Sf-9 cells were transfected with recombinant plasmids using Cellfectin reagent. Firefly luciferase gene located downstream of fusion promoter was considered as a reporter, whereas the activity of the co-transfected Renilla luciferase gene （pGL2-SV40） provides an internal control. This 209 bp region up-regulates the strength of A3 promoter significantly （P〈0.01） when it enters into A3 promoter with respect to the position in sericin 1 gene promoter. This 209-bp fragment was almost functionless when being located upstream of A3 promoter.

Methylation of hMLH1 and hMSH2 promoters in gastric carcinomas

Objective: To study the correlation of the methylation of the promoters of hMLH1 and hMSH2 with microsatellite instability (MSI) in the tissues of gastric carcinomas. Methods: A total of 68 sporadic cases of gastric carcinoma were studied. Ten specimens of normal gastric mucosa served as control. Methylation of hMLHl and hMSH2 was observed with methylation-specific PCR, and MSI analyzed with PCR-based techniques. Results: No methylation of hMLHl and hMSH2 was found in 10 specimens of normal gastric mucosa. Methylation of hMLHl was detected in 11 cases (16. 2%) of gastric cancers and MSI in at least one locus was found in 17 cases (25%) of the 68 with aid of 5 microsatellite markers, in which eight were MSI-H (≥2loci showed instability) nine MSI-L (only one locus showed instability), and fifty-one were MSS (no instability at any marker). The frequency of methylation was significantly high in MSI-H (87. 5%) than in MSI-L (11.1%) and MSS (5. 9%). CP<0. 01 - 0. 001) but there was no difference of methylation frequency between the cases with MSI-L and those with MSS. Conclusion: Methylation of hMLHl promoter is involved to the MSI pathway but not to the loss of heterozygosity (LOH) pathway in gastric carcinogenesis.

Cloning of Promoter of Chinese Bean GRP 1.8 Gene and Characterization of Its Function in Transgenic Tobacco Plants

In order to learn the expression pattern of GRP1 8(glycine rich protein) gene promoter in transgenic plants and to explore its potential application in plant genetic engineering for vascular specific expression of interested genes, GRP 1 8 promoter was amplified by PCR from Chinese bean genomic DNA. The intermediate vector was constructed by inserting vascular specific expression promoter of GRP 1 8 gene in vector pBI 101. The regenerated tobacco plants obtained were analyzed by PCR to select the putative transgenic plants. The histochemical localization of GUS( β D glucosidase) activity indicates that as for that of GRP 1 8 promoter we can confer the vascular specific expression of GUS gene.

Cloning and Sequence Analysis of SLC11A1 Gene Promoter of Three Cattle Breeds in Xinjiang

[Objective]Solute carrier family 11 member 1（SLC11A1）is a major natural resistance candidate gene,which contributes to defense mechanisms of a variety of intracellular bacteria.The SLC11A1 gene promoter sequence of Xinjiang Brown Cattle,Holstein and Simmental were cloned in the test,and promoter sequence difference was analyzed,in order to provide genetic marker-assisted selection for disease-resistant breeding of dairy cattle.[Method]The Genomic DNA was extracted from whole blood collected from three cattle breeds in Xinjiang,and the 5’ flanking region of SLC11A1 gene was amplified by PCR and sequenced.The sequence was analyzed by bioinformatics software CpGplot,RepeatMasker,TFSEARCH,WWW Signal Scan and dual luciferase assay system.[Result]The SLC11A1 gene promoter sequence of 1 463 bp was confirmed,which had promoter activity.No CpG islands were found on promoter sequence.There were four different sites in SLC11A1 gene promoter sequences between Angus from America and three cattle breeds in Xinjiang.Sequence analysis revealed 12 transcription factor binding sites including Sp1,NF1,RelA-p65,GKLF,and CPBP.In promoter region there was an enhancer region（-734- -740）and two short scattered repetitive elements BOV-tA2,MIR3,as well as repeated DNA element Charlie8.[Conclusion]The SLC11A1 gene promoter sequences of three breeds were obtained,which were different from that of Angus.The paper provided a theoretical basis for further studying the influence of SLC11A1 gene polymorphisms on resistance against intracellular bacteria infection.

EFFECTS OF SP1 SITE TO hTERT PROMOTER ACTIVITY AND ITS RESPONSE TO RETINOID ACID

Objective To investigate the junction of Sp1 consensus sites to human telomerase reverse tran-scriptase (hTERT) promoter in different cell lines and in TRA-treated Hela cell. Methods Different length ofhTERT promoter was cloned and inserted into pGL3/basic reporter plasmid. The last four Sp1 sites were deleted byPCR and pGL3B/TRTP413Δ reporter plasmid was constructed. All reporter plasmids were transiently transfected in-to 293, A549, Hela and HepG2 cell lines. 48 h after transfection, luciferase activity was analyzed. hTERT promoteractivity of Hela cell which was treated with trans-retinoid acid (TRA) was tested too. Total RNA of these cells wereextracted and reverse transcript. hTERT mRNA level was analyzed in all tested cells. c-Myc and Sp1 expression wereexamined in Hela cell before and after TRA treatment. U937 was used as a positive control in TRA treatment.Results hTERT was expressed at different level in all tested cell lines. 207bp promoter upstream of transcriptionstart site maintained complete activity. Deletion of last 4 Sp1l sites greatly decreased activity of hTERT promoter, andalmost eliminated its activity in HepG2. TRA increased the activity of different length hTERT promoters in Hela cell,but the activity of Sp1 site-deleted promoter decreased by 3 times. Unlike U937 cell, hTERT expression of Hela cellincreased after TRA treatment, and c-Myc and Sp1 mRNA level were relatively stable. Conclusion Sp1 site wasrequired for transactivation of hTERT promoter and played an important role during TRA treatment.

Study of Transcription Activity of X-Box Binding Protein 1 Gene in Human Different Cell Lines

Human X-box binding protein 1 （XBP1）, an important transcription factor, participates in many signal transduction processes. To further investigate the biological function of XBP1, sequences of XBP1 promoter and its two deletion mutants were first determined using bioinformatic analysis. The report vectors containing XBP1 promoter and its deletion mutants were then constructed, namely, p1-XBPlp, p2-XBPlp, and p3-XBPlp. Each reporter vector was separately transfected into HepG2, L02, K562, SMMC-7721, HSF, and Lipocyte lto Cell line using FuGENE 6 transfection reagents. The activity of chloramphenicol acetyltransferase （CAT） in each group of transfected cells was detected by ELISA assay, which in turn reflects the transcription activity of the XBP1 gene promoter. The activity involving p3-XBPlp was the highest in HepG2, which was 12.4-fold of that of pCAT3-Basic. The activities of p3-XBPlp in K562 and SMMC-7721 were the second and the third highest, which were 10.9-fold and 10.0-fold of that of the pCAT3-Basic, respectively. The CAT activity in L02 was lower than that in the above-mentioned abnormal cell, and no reporter activity was detected in HSF and Ito Cell. The XBP1 transcription and expression in K562, HepG2 and SMMC-7721 were found to be higher than that in L02, HSF and Ito cells, based on the results of real-time RT-PCR and Western blot. The XBP1 transcription and expression in L02, HSF was lower, whereas that in Ito cells was totally lacking. The result was similar to that of CAT-ELISA. Therefore, the XBP1 gene promoter can drive its downstream gene expression and its activity is cell line-dependent. The core sequence of XBP1 promoter was found between -227bp and 66bp sequence. This sequence was closely associated with the transcriptional activity of XBP1 promoter.

CLONING PROMOTER OF HUMAN SATBl GENE AND EFFECT OF ATRA AND CoCl_2 ON ITS ACTIVITY

Objective To explore the structure and activity of SATB1 promoter in different cells, ATRA and CoCl2 effect on its activity. Methods Using luciferase system to assay the promoter activity of human SATB1 gene, three luciferase reporter vectors were constructed which driven by different regions of 5＇ untranslated sequence from human SATB1 gene , called pGL3-SP2946-luc , pGL3-SP1718-luc and pGL3-SP751-luc , and transfected into Jurkat T, K562, U937 and Hela cells transiently using lipofectinamine, the expression activity was detected at different dosage of A TRA and CoCl2treatment for different time course. Results The reporter gene expression from SATB1 promoter were high activity in U937 cell, moderate in Jurkat T cell, low activity in K562 cell and showed no obvious activity in Hela cell, the reporter gene expression from pGL3-SP751-1uc kept on the higher lever in Jurkat T, K562 and U937 cells than the other two vectors. We also found that the repressive effect of CoCI2 on SATBI＇s mRNA expression and the relative luciferase expression from pGL3-SP751-luc in U937 cell was down-regu- lated obviously by ATRA and CoCI2 in the concentration- and time-dependent manners. Conclusion SATB1 pro- rooter drives gene expression with cell-specificity and its core promoter region maybe exist in the - 751 - - 9bp of 5＇ untranslated region of human SATB1 gene. Combined with the experiment result we found before that SATB1 was down-regulated by ATRA in U937, the results imply that STAB1 maybe is down-regulated by ATRA and CoCl2 through its promoter in the differentiation of myeloid cell line-U937.

NUMB maintains bone mass by promoting degradation of PTEN and GLI1 via ubiquitination in osteoblasts

The adaptor protein NUMB is involved in asymmetric division and cell fate determination and recognized as an antagonist of Notch.Previous studies have proved that Notch activation in osteoblasts contributes to a high bone mass. In this study, however, an osteopenic phenotype was found in 9-week-old mice using osteoblastic specific Col1a1–2.3-Cre to ablate both Numb and its homologue Numbl. The trabecular bone mass decreased dramatically while the cortical bone mass was unaffected. Here, the Notch signal was not activated,while the tensin homologue deleted on human chromosome 10(PTEN), which dephosphorylates phosphatidylinositide 3-kinases, was elevated, attenuating protein kinase B(Akt). The ubiquitination assay revealed that NUMB may physiologically promote PTEN ubiquitination in the presence of neural precursor cell-expressed developmentally downregulated protein 4–1. In addition, the deficiency of Numb/Numbl also activated the Hedgehog pathway through GLI1. This process was found to improve the ratio of the receptor activator of nuclear factor-k B ligand to osteoprotegerin, which enhanced the differentiation of osteoclasts and bone resorption. In conclusion, this study provides an insight into new functons of NUMB and NUMBL on bone homeostasis.

Immunization with Cop-1 promotes neuroprotection and neurogenesis after ischemic stroke

Cerebrovascular diseases are considered to be amongst the most serious public health issues,since they are the third leading cause of death（WHO,2014）and the most common cause of disability worldwide.Its monetary significance is evidenced by the economic burden imposed on health care systems,given that the cost of medical care for a patient that has suffered a stroke is around$25,741US dollars every 5 years（Luengo-Fernandez et al.,2012）.A stroke occurs as a result of a disturbance or interruption of cerebral blood flow that significantly reduces the supply of oxygen and glucose to the neural tissue. Consequently, several cell death mechanisms （secondary lesion mechanisms） such as necrosis, excitotoxicity, free radical production and inflammation are triggered （Castillo, 2000）.

FAM64A promotes HNSCC tumorigenesis by mediating transcriptional autoregulation of FOXM1

Head and neck squamous cell carcinoma(HNSCC)still lacks effective targeted treatment.Therefore,exploring novel and robust molecular targets is critical for improving the clinical outcome of HNSCC.Here,we reported that the expression levels of family with sequence similarity 64,member A(FAM64A)were significantly higher in HNSCC tissues and cell lines.In addition,FAM64A overexpression was found to be strongly associated with an unfavorable prognosis of HNSCC.Both in vitro and in vivo evidence showed that FAM64A depletion suppressed the malignant activities of HNSCC cells,and vice versa.Moreover,we found that the FAM64A level was progressively increased from normal to dysplastic to cancerous tissues in a carcinogenic 4-nitroquinoline-1-oxide mouse model.Mechanistically,a physical interaction was found between FAM64A and forkhead box protein M1(FOXM1)in HNSCC cells.FAM64A promoted HNSCC tumorigenesis not only by enhancing the transcriptional activity of FOXM1,but also,more importantly,by modulating FOXM1 expression via the autoregulation loop.Furthermore,a positive correlation between FAM64A and FOXM1 was found in multiple independent cohorts.Taken together,our findings reveal a previously unknown mechanism behind the activation of FOXM1 in HNSCC,and FAM64A might be a promising molecular therapeutic target for treating HNSCC.

Neuregulin 1 isoforms could be an effective therapeutic candidate to promote peripheral nerve regeneration

Traumatic injuries of peripheral nerves represent common casualties and their social impact is considerably high. Although peripheral nerves retain a good regeneration potential, the clinical outcome after nerve lesion is far from being satisfactory and functional recovery is almost never complete, especially in the case of large nerve defects, that result in loss or diminished sensitivity and/or motor activity of the innervated target organs. Therefore, to improve the outcome after nerve damage, or in peripheral neuropathies, there is a need for further research in nerve repair and regeneration to identify factors that promote axonal regrowth, remvelination and target reinnervation.

Enhanced Effects of TRAIL-endostatin-based Double-gene-radiotherapy on Suppressing Growth, Promoting Apoptosis and Inducing Cell Cycle Arrest in Vascular Endothelial Cells

This study examined the effects of TRAIL-endostatin-based gene-radiotherapy on cellu-lar growth, apoptosis and cell cycle progression in human vascular endothelial cells ECV304 in vitro. The expression of TRAIL and endostatin protein in ECV304 cells was detected by ELISA after the transfection of recombinant plasmid pshuttle-Egr1-shTRAIL-shES and X-ray irradiation. Then MTT assay was used for determining the cellular proliferation, and flow cytometry (FCM) plus Annexin V and propidium iodide (PI) double-staining or PI single-staining were employed for the detection of apoptosis and cell cycle progression. The results showed that expression of TRAIL and endostatin protein exhibited a time- and dose-dependent change in ECV304 cells after pshut-tle-Egr1-shTRAIL-shES transfection in conjunction with irradiation. In the TRAIL-endostatin-based single- or double-gene-radiotherapy, the cell viability declined in a time- and dose-dependent manner, the percentage of cells at G2/M phase and apoptotic rate was increased, and the percentage of cells at G0/G1 phase was lowered as compared with those receiving radiotherapy alone. Moreover, TRAIL-endostatin-based double-gene-radiotherapy demonstrated better effects on growth inhibition, promotion of apoptosis and induction of cell cycle arrest in ECV304 cells than single-gene-radiotherapy.

Activation of the Ig la I promoter by the transcription factor Ets-1 triggers Ig lal-Cal germline transcription in epithelial cancer cells

Immunoglobulins （Igs） are known to be synthesized and secreted only by B lymphocytes. Class switch recombination （CSR） is a key event that enables B cells to express Igs, and one of the crucial steps for CSR initiation is the germline transcription of Iggenes. Surprisingly, recent studies have demonstrated that the Iggenes are also expressed in some epithelial cancer cells; however, the mechanisms underlying how cancer cells initiate CSR and express Igs are still unknown. In this study, we confirmed that the Ig la I promoter in cancer cell lines was activated by the Ets- 1 transcription factor, and the activity of the Ig la I promoter and ig lal-C^l germiine transcription were attenuated after knockdown of Ets-1 by specific small interfering RNAs （siRNA）. Furthermore, the expression of Ets-1 and Iga heavy chain in cancer cells was dose dependently upregulated by TGF-I^I. These results indicate that activation of the Ig lal promoter by the transcriotion factor Ets-1 is a critical Dathwav and orovides a novel mechanism for le exoression in non-B cell cancers.

High REDOX RESPONSIVE TRANSCRIPTION FACTOR1 Levels Result in Accumulation of Reactive Oxygen Species in Arabidopsis thaliana Shoots and Roots

Redox Responsive Transcription Factor1 （RRTF1） in Arabidopsis is rapidly and transiently upregulated by H202, as well as biotic- and abiotic-induced redox signals. RRTF1 is highly conserved in angio- sperms, but its physiological role remains elusive. Here we show that inactivation of RRTF1 restricts and overexpression promotes reactive oxygen species （ROS） accumulation in response to stress. Transgenic lines overexpressing RRTF1 are impaired in root and shoot development, light sensitive, and susceptible to Alternaria brassicae infection. These symptoms are diminished by the beneficial root endophyte Piriformospora indica, which reduces ROS accumulation locally in roots and systemi- cally in shoots, and by antioxidants and ROS inhibitors that scavenge ROS. More than 800 genes were detected in mature leaves and seedlings of transgenic lines overexpressing RRTF1; ∽40% of them have stress-, redox-, ROS-regulated-, ROS-scavenging-, defense-, cell death- and related functions. Bioinformatic analyses and in vitro DNA binding assays demonstrate that RRTF1 binds to GCC-box-like sequences in the promoter of RRTFl-responsive genes. Upregulation of RRTF1 by stress stimuli and H202 requires WRKY18/40/60. RRTF1 is co-regulated with the phylogenet- ically related RAP2.6, which contains a GCC-box-like sequence in its promoter, but transgenic lines overexpressing RAP2.6 do not accumulate higher ROS levels. RRTF1 also stimulates systemic ROS accumulation in distal non-stressed leaves. We conclude that the elevated levels of the highly conserved RRTF1 induce ROS accumulation in response to ROS and ROS-producing abiotic and biotic stress signals.

Association of HLA-DQB1 coding region with unexplained recurrent spontaneous abortion

Background DNA analysis has shown a lack of significant compatibility between couples affected by unexplained recurrent spontaneous abortion (URSA) compared with normal fertile couples, 8 although one study that made use of a PCR-sequence-specific oligonucleotide (SSO) method did observe evidence of significant compatibility in the HLA-DQA1 and DQB1 alleles between patients and aborted fetuses. 9 This study was designed to investigate whether URSA were associated with particular DQ alleles or promoter alleles.Methods Thirty-two patients with URSA and 54 women who had had at least one successful pregnancy were included in this study. HLA-DQ genotyping was performed by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The HLA-DQB1 promoter was detected by the SSO and sequence-specific primer (SSP) methods. The DQA1, DQB1, and DQB1 promoter (QBP) gene frequencies in the patients were compared with the gene frequencies in normal controls. The data were analyzed statistically with the χ 2 and Fisher’s exact tests.Results The results showed that the frequency of DQB1 *0604/0605 was significantly higher and the frequency of DQB1 *0501/0502 was significantly lower in the patient group as compared with the normal controls. In addition, the frequencies of the DQA1 *01-DQB1 *0604/0605 and QBP6.2-DQB1 *0604/0605 haplotypes were overrepresented in the patients relative to the controls. Our results did not show any differences between URSA patients and the controls with regard to DQA1 and QBP allele frequencies. Conclusions Our data suggest that URSA is associated with the HLA-DQB1 coding region, and is not associated with its upstream regulatory region. The DQB1 *0604/0605, DQA1 *01-DQB1 *0604/0605, and QBP6.2-DQB1 *0604/0605 haplotypes may confer susceptibility to URSA, while the DQB1 *0501/0502 allele may protect women from URSA.

ABNORMAL SHOOT 6 interacts with KATANIN 1 and SHADE AVOIDANCE 4 to promote cortical microtubule severing and ordering in Arabidopsis

Plant interphase cortical microtubules(cMTs)mediate anisotropic cell expansion in response to environmental and developmental cues.In Arabidopsis thaliana,KATANIN 1(KTN1),the p60 catalytic subunit of the conserved MT-severing enzyme katanin,is essential for cMT ordering and anisotropic cell expansion.However,the regulation of KTN1-mediated cMT severing and ordering remains unclear.In this work,we report that the Arabidopsis IQ67 DOMAIN(IQD)family gene ABNORMAL SHOOT 6(ABS6)encodes a MT-associated protein.Overexpression of ABS6 leads to elongated cotyledons,directional pavement cell expansion,and highly ordered transverse cMT arrays.Genetic suppressor analysis revealed that ABS6-mediated cMT ordering is dependent on KTN1 and SHADE AVOIDANCE 4(SAV4).Live imaging of cMT dynamics showed that both ABS6 and SAV4 function as positive regulators of cMT severing.Furthermore,ABS6 directly interacts with KTN1 and SAV4 and promotes their recruitment to the cMTs.Finally,analysis of loss-of-function mutant combinations showed that ABS6,SAV4,and KTN1 work together to ensure the robust ethylene response in the apical hook of dark-grown seedlings.Together,our findings establish ABS6 and SAV4 as positive regulators of cMT severing and ordering,and highlight the role of cMT dynamics in fine-tuning differential growth in plants.

ANAPHASE PROMOTING COMPLEX/CYCLOSOME-mediated cyclin B1 degradation is critical for cell cycle synchronization in syncytial endosperms

Although it is known that in most angiosperms mitosis in early endosperm development is syncytial and synchronized, it is unclear how the synchronization is regulated. We showed previously that APC11, also named ZYGI, in Arabidopsis activates zygote division by interaction and degradation of cyclin B1. Here, we report that the mutation in APC11/ZYG1 led to unsynchronized mitosis and over-accumulation of cyclin B1-GUS in the endosperm. Mutations in two other APC subunits showed similar defects. Transgenic expression of stable cyclin B1 in the endosperm also caused unsynchronized mitosis. Further, downregulation of APC11 generated multi-nucleate somatic cells with unsynchronized mitotic division. Together, our results suggest that APC/C-mediated cyclin B1 degradation is critical for cell cycle synchronization.

STIL enhances the development of lung adenocarcinoma by regulating the glycolysis pathway

Background:To investigate SCL/TAL 1 interrupting locus(STIL)’s role and prognostic significance in lung adenocarcinoma(LUAD)progression,we examined STIL and E2 promoter binding factor 1(E2F1)expression and their impacts on LUAD prognosis using Gene Expression Profiling Interactive Analysis(GEPIA).Methods:Functional assays including CCK-8,wound-healing,5-ethynyl-2-deoxyuridine(EdU),Transwell assays,and flow cytometry,elucidated STIL and E2F1’s effects on cell viability,proliferation,apoptosis,and migration.Gene set enrichment analysis(GSEA)identified potential pathways,while metabolic assays assessed glucose metabolism.Results:Our findings reveal that STIL and E2F1 are overexpressed in LUAD,correlating with adverse outcomes.It enhances cell proliferation,migration,and invasion,and suppresses apoptosis,activating downstream of E2F1.Silencing E2F1 reversed the promotion effect of the STIL overexpression on cell viability and invasiveness.Importantly,STIL modulates glycolysis,influencing glucose consumption,lactate production,and energy balance in LUAD cells.Conclusion:Our model,incorporating STIL,age,and disease stage,robustly predicts patient prognosis,underscored STIL’s pivotal role in LUAD pathogenesis through metabolic reprogramming.This comprehensive approach not only confirms STIL’s prognostic value but also highlights its potential as a therapeutic target in LUAD.