Participation of an abnormality in the transforming growth factor–β signaling pathway in resistance of malignant glioma cells to growth inhibition induced by that factor

Zhang, Lei; Sato, Eiji; Amagasaki, Kenichi; Nakao, Akihiro; Naganuma, Hirofumi

doi:10.3171/jns.2006.105.1.119

Cited by 29 publications

(26 citation statements)

References 44 publications

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“…However, in contrast to normal EC cells, which demonstrated nuclear targeting of pSMAD2 after TGFb1 stimulation, nuclear pSMAD2 positivity was barely detectable in KRJ-I cells (<7%). These data suggest that TGFb1-mediated signal transduction in a small intestinal carcinoid cell line, as in glioma cell lines, 54 is blocked at the level of SMAD nuclear translocation.…”

Section: Discussionmentioning

confidence: 83%

“…P21 WAF1/CIP1 expression levels are increased in cell lines treated with TGFb1 that have intact TGFb1-mediated cytostatic pathways, 58,59 and may be unaltered in glioma cell lines that have lost this responsiveness. 54 In the current study, p21 WAF1/CIP1 transcription and protein was decreased. KRJ-I cells express time-dependent increases in both transcript and protein expression of c-Myc in response to TGFb1 treatment.…”

Section: Discussionmentioning

confidence: 84%

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Small bowel carcinoid (enterochromaffin cell) neoplasia exhibits transforming growth factor–β1‐mediated regulatory abnormalities including up‐regulation of C‐Myc and MTA1

Kidd

Modlin

Pfragner

et al. 2007

Cancer

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Objective To examine whether and to what extent the intracellular trafficking features of HLA–B*2705, which is associated with the development of spondylarthritis (SpA), differ from those of HLA–B*2709 and HLA–B*0702, which are not associated with SpA. Methods HeLa cells were transfected with complementary DNA encoding for HLA–B proteins fused to Renilla luciferase or yellow fluorescent protein. The subcellular distribution of properly folded and unfolded/misfolded HLA–B proteins was examined by flow cytometry and confocal microscopy of cells labeled with ME1 and HC‐10 antibodies, respectively. HLA–B/HLA–B interactions were monitored in endoplasmic reticulum (ER)– and plasma membrane–enriched subcellular fractions, by bioluminescence resonance energy transfer (BRET). Results All 3 HLA–B alleles displayed a similar distribution pattern (properly folded heavy chain at the cell surface, unfolded/misfolded proteins only in the cytoplasm). By means of BRET, we provided evidence that both HLA–B*2705 and HLA–B*2709 formed more oligomers in the ER and the plasma membrane than did HLA–B*0702. The propensity of HLA–B*2705 to form oligomers in the ER was partly attributable to residue Cys67 of the molecule. For all 3 alleles, increased expression of HLA–B proteins was associated with intracytoplasmic accumulation of unfolded/misfolded proteins and intracellular vesicles, probably corresponding to expanded ER–Golgi intermediate compartments, in which these proteins accumulated together with the stress sensor BiP. Conclusion Our results suggest that the difference in disease susceptibility conferred by HLA–B*2705 and HLA–B*2709 cannot be explained by their different propensity to form dimers or misfolded proteins, thus presumably implicating other, still unknown factors.

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 84%

Small bowel carcinoid (enterochromaffin cell) neoplasia exhibits transforming growth factor–β1‐mediated regulatory abnormalities including up‐regulation of C‐Myc and MTA1

Kidd

Modlin

Pfragner

et al. 2007

Cancer

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“…EI24, a p53-target gene, was lost in invasive breast cancers, and knockdown of EI24 conferred resistance to etoposide treatment in breast cancer cells [51]. SMAD2 expression is lower in glioma cells than in normal astrocytes [52]. Similarly, two genes (EPHX1 and BRD7) are promising targets of miR-10a*.…”

Section: Discussionmentioning

confidence: 99%

miR-195, miR-455-3p and miR-10a∗ are implicated in acquired temozolomide resistance in glioblastoma multiforme cells

Ujifuku¹,

Mitsutake²,

Takakura³

et al. 2010

Cancer Letters

209

137

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Running title: miRNAs and temozolomide resistance in glioblastoma Key words: glioblastoma, resistance, microRNA,, miR-10a*, temozolomide. ABSTRACTTo identify microRNAs (miRNAs) specifically involved in the acquisition of temozolomide (TMZ) resistance in glioblastoma multiforme (GBM), we first established a resistant variant, U251R cells from TMZ-sensitive GBM cell line, U251MG. We then performed a comprehensive analysis of miRNA expressions in U251R and parental cells using miRNA microarrays. miR-195, miR-455-3p and miR-10a* were the three most up-regulated miRNAs in the resistant cells. To investigate the functional role of these miRNAs in TMZ resistance, U251R cells were transfected with miRNA inhibitors consisting of DNA/LNA hybrid oligonucleotides. Suppression of miR-455-3p or miR-10a* had no effect on cell growth, but showed modest cell killing effect in the presence of TMZ. On the other hand, knockdown of miR-195 alone displayed moderate cell killing effect, and combination with TMZ strongly enhanced the effect. In addition, using in silico analysis combined with cDNA microarray experiment, we present possible mRNA targets of these miRNAs. In conclusion, our findings suggest that those miRNAs may play a role in acquired TMZ resistance and could be a novel target for recurrent GBM treatment.

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“…После фосфорилирования белки Smad2,3 формируют гетеромерные комплексы c Smad4, затем мигрируют из цитоплазмы в ядро, где совместно с транскрипционными коактиваторами/корепрессорами (Ski, Sno) регулируют транскрипцию таргетных генов. Smad7 предотвращает TGFb-сигналинг, ингибируя фосфорилирование Smad2,3 [60,61].…”

Section: Tgfb-сигналингunclassified

“…Показано, что экспрессия белков Smad2 и особенно Smad3, а также уровень фосфорилированного Smad2, были значительно ниже в клеточных линиях глиомы по сравнению с другими линиями опухолевых клеток (А549, карцинома лёгкого) или нормальными астроцитами, при этом TGFb-сигналинг не влиял на экспрессию Sno, p21, p15, циклина D1 или CDK4 [61].…”

Section: Tgfb-сигналингunclassified

The role of micro-RNA in the regulation of signal pathways in gliomas

et al. 2017

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Рисунок 1. Два механизма, используемые микро-РНК для регуляции трансляции. Некоторые miRNA способны полностью комплементарно связываться с таргетными мРНК, что вызывает их деградацию. Микро-РНК также могут быть не полностью комплементарны мишеням, тем самым, трансляция блокируется. Адаптировано из [147].

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Participation of an abnormality in the transforming growth factor–β signaling pathway in resistance of malignant glioma cells to growth inhibition induced by that factor

Abstract: These results suggest that the ability to resist TGFbeta-mediated growth inhibition in malignant glioma cells is due to abnormalities in the TGFbeta signaling pathway.

Cited by 29 publications

References 44 publications

Small bowel carcinoid (enterochromaffin cell) neoplasia exhibits transforming growth factor–β1‐mediated regulatory abnormalities including up‐regulation of C‐Myc and MTA1

Small bowel carcinoid (enterochromaffin cell) neoplasia exhibits transforming growth factor–β1‐mediated regulatory abnormalities including up‐regulation of C‐Myc and MTA1

miR-195, miR-455-3p and miR-10a∗ are implicated in acquired temozolomide resistance in glioblastoma multiforme cells

The role of micro-RNA in the regulation of signal pathways in gliomas

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