Phorbol 12-Myristate 13-Acetate Induces Protein Kinase Cη-specific Proliferative Response in Astrocytic Tumor Cells

Hussaini, Isa M.; Karns, Larry R.; Vinton, Griffith; Carpenter, Joan E.; Redpath, Gerard T.; Sando, Julianne J.; VandenBerg, Scott R.

doi:10.1074/jbc.m003203200

Cited by 53 publications

(71 citation statements)

References 39 publications

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“…However, U0126 blocked basal transcription, and reduced PMA-induced proliferation more so than BIM. Together with data previously reported (Hussaini et al, 2000), the data strongly suggest that PMA activation of PKC-Z leads to MEK activation, which targets the transcription factor Elk-1.…”

Section: Resultssupporting

confidence: 84%

“…Pretreatment with BIM alone had no effect on basal levels of transcription or proliferation, it did block the PMA-induced transcriptional activity of Elk-1 and the proliferative response (Figure 5a and b). We have previously shown that antisense directed against PKC-Z reduces PMA-induced proliferation of U251 cells (Hussaini et al, 2000). Collectively, the data suggest that PKC-Z regulates proliferation in U-251, and that the proliferative response involves Elk-1.…”

Section: Resultsmentioning

confidence: 63%

“…PMA increases the mitogenic response in U-251 cells, and inhibits the mitogenic response in U-1242 cells. Furthermore, stable expression of PKC-Z in the U-1242 cells (U-1242-PKC-Z) confers a PMA growth-stimulated phenotype similar to that of the U-251 (Hussaini et al, 2000). These data suggest that the novel PKC-Z isozyme confers an increased proliferative response to mitogenic stimuli.…”

Section: Introductionmentioning

confidence: 79%

“…Expression of PKC-Z correlates with the growth properties of two glioblastoma cell lines: U-251 cells and the stably transfected U-1242-PKC-Z cell line (Hussaini et al, 2000). Furthermore, PKC-Z partially increases cell proliferation via Akt, and the mammalian target of rapamycin (mTOR) (Aeder et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

“…We compared the response to PMA in U-251 cell to that of U-1242 cells. U-251 cells express PKC-Z (Mishima et al, 1994) but the U-1242 line do not (Hussaini et al, 2000). PMA increases the mitogenic response in U-251 cells, and inhibits the mitogenic response in U-1242 cells.…”

Section: Introductionmentioning

confidence: 97%

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The protein kinase C-η isoform induces proliferation in glioblastoma cell lines through an ERK/Elk-1 pathway

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Protein kinase C mediates neurite guidance at an astrocyte boundary

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Identification of novel LncRNA targeting Smad2/PKCα signal pathway to negatively regulate malignant progression of glioblastoma

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et al. 2019

Journal Cellular Physiology

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Glioblastoma multiforme (GBM) is a highly proliferative cancer with generally poor prognosis and accumulating evidence has highlighted the potential of long noncoding RNAs (lncRNAs) in the biological behaviors of glioma cells. This study focused on the identification of lncRNAs to identify targets for possible GBM prognosis. Microarray expression profiling found that 1,759 lncRNAs and 3,026 messenger RNAs (mRNAs) were upregulated, and 1932s lncRNA and 2,979 mRNAs were downregulated in GBM. Bioinformatics analysis and experimental verification identified TCONS_00020456 (TCON) for further analysis. In situ hybridization, along with immunohistochemical and receiver operating characteristic analysis determined TCON (truncation value = 3.5) as highly sensitive and specific in GBM. Grade IV patients with glioma life span with different lncRNA staining scores were analyzed. TCON staining scores below 3.5 indicated poor prognosis (life span ranging from 0.25 to 7 months), even if the glioma was surgically removed. TCON decreased significantly in GBM, and showed a coexpressional relationship with Smad2 and protein kinase C α (PKCα). Overexpression of TCON reduced the proliferation on one hand and migration, invasion on the other. TCON also inhibited epithelial–mesenchymal transformation and glioma progression in vivo, based on a nude mouse tumorigenicity assay. In addition, we predicted a potential binding site and intersection that microRNAs targeting Smad2, PKCα, and TCON through RACE pretest and bioinformatics analysis. Taken together, TCON, regarded as oncosuppressor, targeting the Smad2/PKCα axis plays a novel role in inhibiting the malignant progression of glioma. Moreover, it also demonstrates that the level of TCON can be used as a prognostic and diagnostic biomarker for GBM.

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Phorbol 12-Myristate 13-Acetate Induces Protein Kinase Cη-specific Proliferative Response in Astrocytic Tumor Cells

Cited by 53 publications

References 39 publications

The protein kinase C-η isoform induces proliferation in glioblastoma cell lines through an ERK/Elk-1 pathway

The protein kinase C-η isoform induces proliferation in glioblastoma cell lines through an ERK/Elk-1 pathway

Protein kinase C mediates neurite guidance at an astrocyte boundary

Identification of novel LncRNA targeting Smad2/PKCα signal pathway to negatively regulate malignant progression of glioblastoma

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