Sp1 is essential for regulating the CD147 gene expression in human lung cancer.

Sp1 was found to activate the transcription of TAp73gamma in lung cancer via highly conserved Sp1-binding sites on the p73 P1 promoter. TAp73gamma and Sp1 are co-overexpressed both in vitro and in situ in lung cancer.

Results demonstrate that Sp1 and Sp3 transcription factors are the primary determinants for activating basal transcription of the ABCG2 gene and play an important role in maintaining the side population phenotype of lung cancer cells.

In the early stages of lung cancer progression, Sp1 stimulates miR-182 expression, which in turn decreases FOXO3 expression.

Study concludes that suppression of lung cancer cell invasion by LKB1 through downregulation of TF and VEGF may partly depend on its inhibitory effect on the transcription factor Sp1.

Sp1 transcriptionally regulates BRK1 expression in non-small cell lung cancer cells. Sp1 can bind to the promoter area of BRK1 gene.

we found that miR-27 suppressed growth and invasion of non-small cell lung cancer cells partially by targeting Sp1

The data suggest that upregulation of MALAT1 was mediated by the transcription factor Sp1 in A549 lung cancer cells

Results have shown crosstalk among the EGFR cascade and Sp1 and DPD expressions in EGFR mutant non-small-cell lung cancer cell lines. EGF-induced Sp1 up-regulation resulted in both DPYD mRNA and DPD protein expressions.

miR-326 can restore CDDP chemosensitivity in the human lung adenocarcinoma cells by targeting SP1, and HOTAIR upregulate the expression of miR-326 target gene SP1.

miR-29c overexpression could abrogate the tumor progression and inhibit the Sp1/TGF-beta expressions in vivo, indicating that miR-29c could be a tumor suppressor and repress the Sp1/TGF-beta axis-induced EMT in lung cancer.

Data indicate that DNMT3A allele G of rs1550117 was associated with an increased risk of non-small cell lung cancer (NSCLC) susceptibility and binding affinity of transcription repressor SP1.

E6 upregulation of hTERT by downregulated LKB1 and upregulated SP1 in lung cancer cells. These results indicated that E6 played a predominant role in the regulation of telomerase activation and may be a valuable therapeutic targets for HPV-related cancer.

Low expression levels of Sp1 and Nm23-H1 are correlated with poor prognosis in patients with lung cancer. Further data indicated that lung cancer patients with higher levels of Sp1 and Nm23-H1 also exhibited high levels of hnRNPA2/B1, suggesting a positive correlation between the levels of Sp1, Nm23-H1 and hnRNPA2/ B1 during lung cancer formation.

Taken together, these data clearly show that FKBP3/Sp1/HDAC2/p27 control cell proliferation during non-small cell lung cancer development.

Results show that C-terminal domain of SP1 interacts malat1 M5 domain which regulates its expression and stability. In turn, SP1 promotes malat1 transcription, thus forming a positive feedback loop in lung adenocarcinoma cells.

These data demonstrate that miR-326/Sp1/KLF3 regulatory axis is involved in the development of lung cancer. miR-326 could bind to 3'UTR of Sp1 but not KLF3 and decreased the accumulation of Sp1, which further indirectly reduced KLF3 expression and inactivated JAK2/STAT3 and PI3K/AKT signaling pathways in vitro and in vivo.

These findings suggest that the transcription of the b4GalT3 gene is regulated by differential DNA binding of Sp3 and Sp1 in neuroblastoma and lung cancer. The increased expression of b4GalT3 in neuroblastoma may be ascribed to the enhanced expression of Sp3, which is observed for various cancers.

SP1 role in the non small cell lung cancer.MIR31HG is a direct target of SP1.

SP1-mediated overexpression of lncRNA LINC01234 facilitates non-small-cell lung cancer progression by regulating OTUB1 expression.

Knockdown of SP1/Syncytin1 axis inhibits the proliferation and metastasis through the AKT and ERK1/2 signaling pathways in non-small cell lung cancer.

Long noncoding RNA LINC00657 induced by SP1 contributes to the non-small cell lung cancer progression through targeting miR-26b-5p/COMMD8 axis.

SP1-regulated LINC01638 promotes proliferation and inhibits apoptosis in non-small cell lung cancer.

The SP1 mediated EPO-R expression played an essential role in hypoxia-induced non-small-cell lung carcinoma cell proliferation.

Results found the expression of Sp1 and PDSS2 are negatively correlated, and higher Sp1 expression with low PDSS2 expression is significantly associated with poor prognosis in lung cancer. Further data strongly suggest the essential role of Sp1 in maintaining the basic constitutive expression of PDSS2, and the pathogenic implication of Sp1-mediated PDSS2 transcriptional repression in lung cancer cells.

[Regulation of IL33 Gene expression by SP1 and Foxa1 in Breast and lung cancer Cells].

Sp1 level accumulated strongly in early stage and then declined in late stage, which is important for lung cancer cell proliferation and metastasis during tumorigenesis.