scholarly journals PUROMYCIN RESISTANCE IN HAPLOID AND HETEROPLOID FROG CELLS: GENE OR MEMBRANE DETERMINED?

1971 ◽  
Vol 51 (3) ◽  
pp. 742-751 ◽  
Author(s):  
Liselotte Mezger-Freed
Keyword(s):  
Membrane Permeability ◽  
Gene Mutation ◽  
Cell Lines ◽  
Colony Formation ◽  
Cell Populations ◽  
Resistant Phenotype ◽  
Mutagen Treatment ◽  
Different Levels

The frequency of colony formation in monolayers of cultured frog cell lines treated with puromycin was compared in (a) haploid and heteroploid lines and (b) mutagen-treated and nontreated haploid lines. Evidence that resistant colonies result from gene mutation was negative, since the colony frequency is independent of both ploidy and mutagen treatment. A study of five frog cell lines showed that colony formation in puromycin depends on (a) the concentration of puromycin, (b) preselection of the population with puromycin, and, particularly, (c) the capacity of the treated population to survive some exposure to puromycin. One haploid and one heteroploid strain showing stable resistance to puromycin have been isolated; comparison of those variants with sensitive populations has shown that resistance to puromycin is correlated with the cells' capacity to exclude the drug. The evidence for different levels of membrane permeability, combined with evidence for many degrees of resistance among and within cell populations, suggests a model of self-determining membrane units. The evolution of a resistant phenotype may result from changes in the proportion of specific units in the membrane population.

scholarly journals Cancer stem cells and cisplatin‐resistant cells isolated from non‐small‐lung cancer cell lines constitute related cell populations

2014 ◽  
Vol 3 (5) ◽  
pp. 1099-1111 ◽  
Author(s):  
Blanca D. Lopez‐Ayllon ◽  
Veronica Moncho‐Amor ◽  
Ander Abarrategi ◽  
Inmaculada Ibañez Cáceres ◽  
Javier Castro‐Carpeño ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Cell Populations ◽  
Lung Cancer Cell ◽  
Related Cell ◽  
Resistant Cells

mdr1 Ribozyme mediated reversal of the multi-drug resistant phenotype in human lung cell lines

1996 ◽  
Vol 19 (3) ◽  
pp. 199-205 ◽  
Author(s):  
Carmel Daly ◽  
Seamus Coyle ◽  
Shirley McBride ◽  
Lorraine O'Driscoll ◽  
Noel Daly ◽  
...  
Keyword(s):  
Cell Lines ◽  
Human Lung ◽  
Drug Resistant ◽  
Resistant Phenotype ◽  
Drug Resistant Phenotype

A constitutively active ErbB4 mutant inhibits drug-resistant colony formation by the DU-145 and PC-3 human prostate tumor cell lines

2003 ◽  
Vol 192 (1) ◽  
pp. 67-74 ◽  
Author(s):  
Eric E Williams ◽  
Laurie J Trout ◽  
Richard M Gallo ◽  
Sarah E Pitfield ◽  
Ianthe Bryant ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Lines ◽  
Colony Formation ◽  
Prostate Tumor ◽  
Human Prostate ◽  
Drug Resistant ◽  
Tumor Cell Lines ◽  
Human Prostate Tumor ◽  
Prostate Tumor Cell ◽  
Constitutively Active

Downregulation of Sulfiredoxin (Srx) Suppressed Cell Proliferation Migration and Invasion Through Inhibiting Extracellular Signal-Regulated Kinase/Nrf2 Pathway in Hepatocellular Carcinoma

2021 ◽  
Vol 11 (11) ◽  
pp. 2137-2145
Author(s):  
Xuejuan Zhu ◽  
Danqian Lu
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Colony Formation ◽  
Migration And Invasion ◽  
Related Factor ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Nrf2 Signaling Pathway

Background: Sulfiredoxin (Srx) has been identified to play important roles in the development of various cancers. However, the precise effects and underlying mechanism of Srx on the progression of HCC are far from being fully understood. Materials and Methods: The abundances of Srx in THLE-2 cell and HCC cell lines were determined by western blot and RT-qPCR. Next, SK-Hep-1 cells were transfected with shRNA-Srx or shRNA-NC and treated with TBHQ (an extracellular signal-regulated kinase (ERK) activator) for functional experiments. Then, CCK8 and colony formation assays were used to determine cell proliferation and clone-forming abilities in vitro. Cell migration and invasion were assessed via wound healing and transwell assays. The expression of MMP2, MMP9 and key members in ERK/nuclear factor E2 related factor (Nrf2) signaling pathway was detected by performing western blot analysis. Results: We reported evidence that Srx was frequently up-regulated in HCC cell lines. Srx interference constrained cell proliferation, colony formation rate, migration and invasion of SK-Hep-1 cells. Moreover, mechanistic investigations indicated that Srx interference significantly inhibited the activation of ERK/Nrf2 signaling pathway, and ERK activator TBHQ can reverse the functions of Srx interference in SK-Hep-1 cells. Conclusion: Overall, Downregulation of Srx might impede HCC progression by suppressing ERK/Nrf2 signaling pathway. Findings in the current study reported the functional involvement and molecular mechanism of Srx in HCC, suggesting that Srx might have a potential therapeutic value in HCC treatment.

CBIO-15. LOSS OF WILLIAMS SYNDROME TRANSCRIPTION FACTOR (WSTF) LEADS TO IMPROVED TEMOZOLOMIDE SENSITIVITY IN HUMAN GLIOBLASTOMA CELLS IRRESPECTIVE OF MGMT EXPRESSION

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi30-vi30
Author(s):  
Katharina Sarnow ◽  
Stephanie Schwab ◽  
Oline Rio ◽  
Joydeep Mukherjee ◽  
Rolf Bjerkvig ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Lines ◽  
Williams Syndrome ◽  
Colony Formation ◽  
Dna Methyltransferase ◽  
Guide Rna ◽  
Methylguanine Dna Methyltransferase ◽  
Development Of Resistance ◽  
Dna Repair Protein ◽  
Underlying Mechanisms

Abstract BACKGROUND The prognosis for glioblastoma multiforme (GBM) patients is poor with a median survival of approximately 15 months. The DNA repair protein O 6-methylguanine-DNA methyltransferase (MGMT) counteracts the effects of temozolomide (TMZ) chemotherapy and is thus associated with poor outcome in GBM patients. Williams Syndrome Transcription Factor (WSTF) has been suggested to regulate the DNA damage response pathway (DDR) in both an indirect (through chromatin remodeling) and direct manner (by phosphorylating H2AX at Tyr142). However, whether WSTF has any role in the development of resistance against chemotherapy through its functions in the DDR in GBMs, is so far unknown. In this study, we investigated whether a loss of WSTF sensitizes different MGMT-proficient and -deficient GBM cell lines to TMZ treatment. METHODS We generated WSTF knockout clones from both MGMT-proficient (LN18, T98G) and -deficient GBM cell lines (U-251) using CRISPR/Cas9 gene-editing technology with lentiviral vectors. The PCR-based screening results combined with the T7 endonuclease mismatch assay for bi-allelic monoclonal knockouts were verified via sequencing and immunoblotting to identify candidate knockout clones. Colony formation assays were performed to determine the survival ability in response to TMZ treatment. Statistical analysis was performed using two-way ANOVA. RESULTS WSTF knockout clones showed a significant decrease in colony formation after TMZ-treatment compared to the corresponding control groups (non-target single guide RNA) (LN18: Clone 59 vs control: p= 0.0456, T98G: All three studied clones vs control: p< 0.0001, U-251: Clone 7/35.1/70.2 vs control: p< 0.0001/p= 0.0107/p= 0.0119). CONCLUSION WSTF is an important factor in both MGMT de- and proficient GBM cell lines for response against TMZ chemotherapy. The loss of WSTF leads to a significantly increased TMZ sensitivity in clinically relevant concentrations for all the studied cell lines. Ongoing studies are investigating the underlying mechanisms and potential alterations in the DDR pathway caused by WSTF loss.

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