Differential Repair of Radiation-Induced DNA Damage in Cells of Human Squamous Cell Carcinoma and the Effect of Caffeine and Cysteamine on Induction and Repair of DNA Double-Strand Breaks

1994 ◽  
Vol 140 (2) ◽  
pp. 153 ◽  
Author(s):  
M. F. M. A. Smeets ◽  
E. H. M. Mooren ◽  
A. H. A. Abdel-Wahab ◽  
H. Bartelink ◽  
A. C. Begg
Keyword(s):  
Dna Damage ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Strand Breaks ◽  
Human Squamous Cell Carcinoma ◽  
Radiation Induced ◽  
In Cells

Differential retention of tumor- and differentiation-suppressor functions in cells derived from a human squamous cell carcinoma

1992 ◽  
Vol 5 (4) ◽  
pp. 278-285 ◽  
Author(s):  
Deborah R. Jaffe ◽  
Yvonne Montero-Puerner ◽  
Michael A. Beckett ◽  
Janet M. Cowan ◽  
Ralph R. Weichselbaum ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Human Squamous Cell Carcinoma ◽  
Differential Retention ◽  
In Cells

Intracellular accumulation and DNA damage persistence as determinants of human squamous cell carcinoma hypersensitivity to the novel camptothecin ST1968

2008 ◽  
Vol 44 (9) ◽  
pp. 1332-1340 ◽  
Author(s):  
Claudio Pisano ◽  
Valentina Zuco ◽  
Michelandrea De Cesare ◽  
Valentina Benedetti ◽  
Loredana Vesci ◽  
...  
Keyword(s):  
Dna Damage ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
The Novel ◽  
Intracellular Accumulation ◽  
Human Squamous Cell Carcinoma

scholarly journals Clustered DNA Double-Strand Breaks: Biological Effects and Relevance to Cancer Radiotherapy

Genes ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 99 ◽  
Author(s):  
Jac A. Nickoloff ◽  
Neelam Sharma ◽  
Lynn Taylor
Keyword(s):  
Dna Damage ◽  
Dna Lesions ◽  
Double Strand Breaks ◽  
Single Strand ◽  
Dna Double Strand Breaks ◽  
Strand Breaks ◽  
High Let Radiation ◽  
High Let ◽  
Radiation Induced ◽  
Clustered Dna Damage

Cells manage to survive, thrive, and divide with high accuracy despite the constant threat of DNA damage. Cells have evolved with several systems that efficiently repair spontaneous, isolated DNA lesions with a high degree of accuracy. Ionizing radiation and a few radiomimetic chemicals can produce clustered DNA damage comprising complex arrangements of single-strand damage and DNA double-strand breaks (DSBs). There is substantial evidence that clustered DNA damage is more mutagenic and cytotoxic than isolated damage. Radiation-induced clustered DNA damage has proven difficult to study because the spectrum of induced lesions is very complex, and lesions are randomly distributed throughout the genome. Nonetheless, it is fairly well-established that radiation-induced clustered DNA damage, including non-DSB and DSB clustered lesions, are poorly repaired or fail to repair, accounting for the greater mutagenic and cytotoxic effects of clustered lesions compared to isolated lesions. High linear energy transfer (LET) charged particle radiation is more cytotoxic per unit dose than low LET radiation because high LET radiation produces more clustered DNA damage. Studies with I-SceI nuclease demonstrate that nuclease-induced DSB clusters are also cytotoxic, indicating that this cytotoxicity is independent of radiogenic lesions, including single-strand lesions and chemically “dirty” DSB ends. The poor repair of clustered DSBs at least in part reflects inhibition of canonical NHEJ by short DNA fragments. This shifts repair toward HR and perhaps alternative NHEJ, and can result in chromothripsis-mediated genome instability or cell death. These principals are important for cancer treatment by low and high LET radiation.

Characterization of the Eugenol Effects on the Bioenergetic Profile of SCC-4 Human Squamous Cell Carcinoma Cell Line

2018 ◽  
Vol 69 (9) ◽  
pp. 2567-2570 ◽  
Author(s):  
Oana M. Duicu ◽  
Ioana Z. Pavel ◽  
Florin Borcan ◽  
Danina M. Muntean ◽  
Adelina Cheveresan ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Line ◽  
Squamous Cell ◽  
Carcinoma Cell ◽  
Carcinoma Cell Line ◽  
Squamous Cell Carcinoma Cell ◽  
Human Squamous Cell Carcinoma ◽  
Extracellular Flux ◽  
Transport Chain

Eugenol (EU), the active ingredient in clove oil, is commonly used as successful therapeutic compound in dentistry due to its antiseptic and anti-inflammatory effects. Recent research studies suggest that eugenol has also a potential anti-cancer effect. This study was thereby purported to assess the effects of EU on the bioenergetic profile of the SCC-4 human squamous cell carcinoma cell line. To this aim, SCC-4 cells were treated for 24 hours with free EU and EU incorporated in polyurethane structures (50 �M each). Oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) were measured using the Seahorse XF-24e extracellular flux analyzer (Agilent Technologies Inc.). Analysis of the SCC-4 bioenergetic profile was performed in the presence of the classic modulators of the electron transport chain: oligomycin, FCCP, and antimycin A+rotenone. Our data showed that cells stimulated with free EU induced a decrease of OCR linked parameters and an increase of ECAR, effects that were abolished by the incorporation of EU in polyurethane structures. In conclusion, free eugenol elicits inhibitory effects on mitochondrial respiration in the SCC-4 cell line, a result that might be suggestive for its anti-tumoral effects.

Corilagin Inhibits Esophageal Squamous Cell Carcinoma by Inducing DNA Damage and Down-Regulation of RNF8

2019 ◽  
Vol 19 (8) ◽  
pp. 1021-1028 ◽  
Author(s):  
Fanghua Qiu ◽  
Lifang Liu ◽  
Yu Lin ◽  
Zetian Yang ◽  
Feng Qiu
Keyword(s):  
Cell Proliferation ◽  
Dna Damage ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cell Apoptosis ◽  
Cell Counting ◽  
Antitumor Effects

Background:Esophageal squamous cell carcinoma (ESCC), the most prevalent histologic subtype of esophageal cancer, is an aggressive malignancy with poor prognosis and a high incidence in the East. Corilagin, an active component present in Phyllanthus niruri L., has been shown to suppress tumor growth in various cancers. However, the effects of corilagin on ESCC and the mechanisms for its tumor suppressive function remain unknown.Methods:Cell proliferation was measured by Cell Counting Kit-8 assay and colony formation assays. Annexin V/PI double-staining was performed to assess cell apoptosis. Immunofluorescence staining and western blotting were used to evaluate the protein expression. A xenograft mice model was used to assess the in vivo antitumor effects of corilagin alone or in combination with cisplatin.Results:We for the first time showed that corilagin was effectively able to inhibit ESCC cell proliferation and induce cell apoptosis. Additionally, our results validated its antitumor effects in vivo using a xenograft mouse model. Mechanistically, we found that corilagin caused significant DNA damage in ESCC cells. We found that corilagin could significantly attenuate the expression of the E3 ubiquitin ligase RING finger protein 8 (RNF8) through ubiquitin-proteasome pathway, leading to the inability of DNA damage repair response and eventually causing cell apoptosis. Furthermore, we also showed that corilagin substantially enhanced the antitumor effects of chemotherapy drug cisplatin both in vitro and in vivo.Conclusion:Our results not only provided novel and previously unrecognized evidences for corilagin-induced tumor suppression through inducing DNA damage and targeting RNF8 in ESCC, but also highlighted that corilagin might serve as an adjunctive treatment to conventional chemotherapeutic drugs in ESCC patients.

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