Influence of XRCC4 expression by breast cancer cells on ipsilateral recurrence after breast-conserving therapy

Kitagawa, M.; Someya, Masanori; Hasegawa, Tomokazu; Mikami, Toshihiko; Asaishi, Kazuaki; Hasegawa, Tadashi; Matsumoto, Yoshihisa; Kutomi, Goro; Takemasa, Ichiro; Sakata, Koh‐ichi

doi:10.1007/s00066-019-01468-z

Cited by 6 publications

(9 citation statements)

References 30 publications

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“…Also, in studies on gastric and breast cancerous tissues, an increase in the XRCC4 gene expression was reported (21,22). Kitagawa et al introduced the expression of the XRCC4 gene as a biomarker to detect the recurrence of breast cancer (22). Overexpression of the DCLRE1C gene, which rises through recruitment of NHEJ repair pathway, was previously reported in lung cancer (23).…”

Section: Discussionmentioning

confidence: 97%

“…It has also been suggested increased expression is because of the ine ciency of the HR repair pathway (20). Also, in studies on gastric and breast cancerous tissues, an increase in the XRCC4 gene expression was reported (21,22). Kitagawa et al introduced the expression of the XRCC4 gene as a biomarker to detect the recurrence of breast cancer (22).…”

Section: Discussionmentioning

confidence: 99%

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Helicobacter pylori Infection Mediates Transcriptional Alteration of Genes Involved in DNA Damage Response

Rajaei

Ghameshlou

Shirkoohi

et al. 2022

Preprint

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Background: Gastritis is among the most common human diseases worldwide. Although the involvement of Helicobacter pylori infection as a class I human carcinogen for gastric cancer progression is accepted, it is not well known how gastritis progression to atrophy and stomach cancer occurs. In this case-control study, the potential link of H. pylori infection with alteration in the transcription of genes involved in DNA Damage Response pathways was investigated among the patients with gastritis. Methods: To measure the difference in relative mRNA expression level of ATM, CHEK2, TP53, DCLRE1C, POLM, XRCC4 genes between H. pylori infected and non-infected patients, gastric biopsies of 30 H. pylori infected patients with moderate chronic gastritis and 30 non-infected patients with mild chronic gastritis were analyzed. Results: Up-regulation of genes linked to non-homologous end joining (NHEJ) pathway (DCLRE1C, POLM, and XRCC) was shown in 40% (8.44 fold ±13.91), 63.33% (15.72 fold ±33.08) and 50% (9.99 fold ±21.55), respectively, and also to DDR pathway (ATM, CHEK2 and TP53) in 33% (2.42 fold ±3.17), 40% (2.86 fold ±3.61) and 50% (5.00 fold ±6.52), respectively. No correlation was detected among alteration in the transcription level of the studied genes and age or gender.Conclusion: Our results provide new data that may support the potential involvement of H. pylori infection in the activation of genes involved in DNA damage response, mainly through non-homologous end joining DNA repair system that might be linked to mutagenesis in the pre-cancerous gastric tissue.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori Infection Mediates Transcriptional Alteration of Genes Involved in DNA Damage Response

Rajaei

Ghameshlou

Shirkoohi

et al. 2022

Preprint

View full text Add to dashboard Cite

show abstract

“…Also, in studies on gastric and breast cancerous tissues, an increase in the XRCC4 gene expression was reported (20,21). Kitagawa et al introduced the expression of the XRCC4 gene as a biomarker to detect the recurrence of breast cancer (21). Overexpression of the DCLRE1C gene, which rises through recruitment of NHEJ repair pathway, was previously reported in lung cancer (22).…”

Section: Discussionmentioning

confidence: 97%

“…It has also been suggested increased expression is because of the ine ciency of the HR repair pathway (19). Also, in studies on gastric and breast cancerous tissues, an increase in the XRCC4 gene expression was reported (20,21). Kitagawa et al introduced the expression of the XRCC4 gene as a biomarker to detect the recurrence of breast cancer (21).…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori Infection Mediates Transcriptional Alteration of Genes Involved in DNA Damage Response

Rajaei

Ghameshlou

Shirkoohi

et al. 2022

Preprint

View full text Add to dashboard Cite

Background: Gastritis is among the most common human diseases worldwide. Although the involvement of Helicobacter pylori infection as a class I human carcinogen for gastric cancer progression is accepted, it is not well known how gastritis progression to atrophy and stomach cancer occurs. In this case-control study, the potential link of H. pylori infection with alteration in the transcription of genes involved in DNA Damage Response pathways was investigated among the patients with gastritis. Methods: To measure the difference in relative mRNA expression level of ATM, CHEK2, TP53, DCLRE1C, POLM, XRCC4 genes between H. pylori infected and non-infected patients, gastric biopsies of 30 H. pylori infected patients with moderate chronic gastritis and 30 non-infected patients with mild chronic gastritis were analyzed. Result: Up-regulation of genes linked to non-homologous end joining (NHEJ) pathway (DCLRE1C, POLM, and XRCC) was shown in 40% (8.44 fold ±13.91), 63.33% (15.72 fold ±33.08) and 50% (9.99 fold ±21.55), respectively, and also to DDR pathway (ATM, CHEK2 and TP53) in 33% (2.42 fold ±3.17), 40% (2.86 fold ±3.61) and 50% (5.00 fold ±6.52), respectively. No correlation was detected among alteration in the transcription level of the studied genes and age or gender.Conclusion: Our results provide new data that may support the potential involvement of H. pylori infection in the activation of genes involved in DNA damage response, mainly through non-homologous end joining DNA repair system that might be linked to mutagenesis in the pre-cancerous gastric tissue.

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“…X-ray repair cross complementing 4 (XRCC4), an important DNA repair gene involved in nonhomologous end-joining (NHEJ) repair pathway, plays a scaffold function via stabilizing and localizing DNA repair enzymes LIG IV, Ku70/80 heterodimer, and the DNA-dependent protein kinase (DNA-PK) catalytic subunit (DNA-PKcs) in the ends of DNA double-stranded breaks (DSBs) during NHEJ [15,16]. In the past decades, growing reports have exhibited that the abnormal structures and functions of XRCC4 may alter the capacity of DNA repair and ultimately result in human diseases [17][18][19][20][21][22]. Several recent studies have also shown that the genetic alterations in the coding regions of XRCC4 can modify hepatocellular carcinoma (HCC) risk and prognosis [23][24][25][26][27].…”

Section: Introductionmentioning

confidence: 99%

X-Ray Repair Cross Complementing 4 (XRCC4) Genetic Single Nucleotide Polymorphisms and the Liver Toxicity of AFB1 in Hepatocellular Carcinoma

Deng¹,

Wu²,

Huang³

et al. 2020

Aflatoxin B1 Occurrence, Detection and Toxicological Effects

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Our previous reports have shown that the genetic single-nucleotide polymorphisms (GSNPs) in the DNA repair gene X-ray repair cross complementing 4 (XRCC4) are involved in the carcinogenesis of hepatocellular carcinoma (HCC) induced by aflatoxin B1 (AFB1). However, the effects of GSNPs in the coding regions of XRCC4 on hepatic toxicity of AFB1 have been less investigated. We conducted a hospital-based clinic tissue samples with pathologically diagnosed HCC (n = 380) in a high AFB1 exposure area to explore the possible roles of GSNPs in the coding regions of XRCC4 in AFB1-induced HCC using liver toxicity assays. A total of 143 GSNPs were included in the present study and genotyped using the SNaPshot method, whereas the liver toxicity of AFB1 was evaluated using AFB1-DNA adducts in the tissues with HCC. In the clinicopathological samples with HCC, the average adduct amount is 2.27 AE 1.09 μmol/mol DNA. Among 143 GSNPs of XRCC4, only rs1237462915, rs28383151, rs762419679, rs766287987, and rs3734091 significantly increased the levels of AFB1-DNA adducts. Furthermore, XRCC4 GSNPs (including rs28383151, rs766287987, and rs3734091) also increased cumulative hazard for patients with HCC. These results suggest that the liver toxicity of AFB1 may be modified by XRCC4 GSNPs.

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Influence of XRCC4 expression by breast cancer cells on ipsilateral recurrence after breast-conserving therapy

Cited by 6 publications

References 30 publications

Helicobacter pylori Infection Mediates Transcriptional Alteration of Genes Involved in DNA Damage Response

Helicobacter pylori Infection Mediates Transcriptional Alteration of Genes Involved in DNA Damage Response

Helicobacter pylori Infection Mediates Transcriptional Alteration of Genes Involved in DNA Damage Response

X-Ray Repair Cross Complementing 4 (XRCC4) Genetic Single Nucleotide Polymorphisms and the Liver Toxicity of AFB1 in Hepatocellular Carcinoma

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