Interestingly, the expression of gli target genes in some glioma cell lines was observed together with a high level of their transcriptional repressor, Gli3R.
Previously, we discovered a novel form of cancer drug resistance where the Glioma-associated protein 1 (GLI1) elevates UGT1A glucuronidation enzymes, thereby glucuronidating cytarabine and ribavirin, leading to resistance in leukemia patients.
In the present study, the expression of PLCε and glioma‑associated homolog (Gli)‑1/Gli‑2 in benign prostatic hyperplasia (BPH), PCa and CRPC tissues and cells was investigated, and the correlations between PLCε and Gli‑1/Gli‑2 in CRPC tissues and cell lines were further explored.
The protein levels of sonic hedgehog (Shh), glioma‑associated oncoprotein 1 (Gli1) and Smoothened (Smo) in nicotine‑induced Hh signaling were also detected.
Finally, we show that GLI inhibition increases apoptosis in glioma stem-like cells by up to 6.8-fold in combination with TMZ, and this reduces the size and number of neurospheres grown from glioma stem-like cells.
Signal transducer and activator of transcription 3 (STAT3), glioma oncogene homolog 1 (GLI1), and truncated GLI1 (tGLI1) are oncogenic transcription factors playing important roles in breast cancer. tGLI1 is a gain-of-function GLI1 isoform.
However, the isoforms PTCH1-1B and PTCH1-Δ10 inhibited SMO and the pathway transcription factor glioma 1 (GLI1) to a greater extent than did PTCH1-Δ15.
We demonstrated that down-regulation of the transcription factor glioma-associated protein 1 (GLI1) in AA-treated cells is the underlying mechanism controlling BCL2, BFL1/A1, and 4-1BB expression.
Therefore, our results suggest that there is a potential nexus of Shh-Gli1-BMI1 cell signaling to regulate MRP1 and to promote chemoresistance in glioma.
The transcription factors glioma-associated oncogene homolog 1 (GLI1), a primary marker of Hedgehog pathway activation, and Forkhead box M1 (FOXM1) are aberrantly activated in a wide range of malignancies, including glioma.
The present study demonstrates that combined treatment with siRNA-Gli1 and BCNU significantly inhibits the proliferation and promotes the apoptosis of glioma U251 cells, possibly by the up-regulation of Bax and the down-regulation of Bcl-2.
Here we identify a novel form of drug resistance to ribavirin and Ara-C. We observe that the sonic hedgehog transcription factor glioma-associated protein 1 (GLI1) and the UDP glucuronosyltransferase (UGT1A) family of enzymes are elevated in resistant cells.
By examination of glioma tissue specimens from 65 patients, we found that the survival of glioma patients was closely correlated with the expression of both Shh by endothelial cells and Gli1 by perivascular glioma cells.
Activation of the Hedgehog (HH) pathway and increased expression of its downstream effector GLI1 are driving factors of glioma tumorigenicity and glioma stem cell (GSC) biology.
Additionally, cyclopamine was used to inhibit the HH signaling activity as an indirect approach to decrease Gli1 expression, and we observed that cyclopamine exclusively inhibited cell growth in HH-pathway-active glioma cell lines.