Tyrosine kinase receptor TIE-1 mediates platinum resistance by promoting nucleotide excision repair in ovarian cancer

Ishibashi, Masayoshi; Toyoshima, Masafumi; Zhang, Xuewei; Hasegawa-Minato, Junko; Shigeta, Shogo; Usui, Toshinori; Kemp, Christopher J.; Grandori, Carla; Kitatani, Kazuyuki; Yaegashi, Nobuo

doi:10.1038/s41598-018-31069-2

Cited by 23 publications

(23 citation statements)

References 38 publications

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“…It is hardly surprising, therefore, that upregulation of NER mediates resistance to cisplatin-based therapy [2,157]. Ishibashi et al reported that in OvC cell lines, tyrosine kinase with immunoglobulin-like and EGF like domains 1 (TIE1) promotes XPC-dependent NER and this leads to decreased susceptibility to cisplatin-induced cell death [158]. Last but not least, a study in 559 EOC patients showed an association of ERCC1 polymorphisms rs11615 and rs3212986 with cisplatin resistance Zhao et al analysed 17 SNPs in NER genes XPA, XPC, XPD/ERCC2, XPF/ERCC4, XPG, and ERCC1 in 89 OvC cases and 356 controls, and their results suggested that ERCC1, XPC, and XPD/ERCC2 may be linked to OvC susceptibility [154].…”

Section: Nucleotide Excision Repairmentioning

confidence: 99%

DNA Repair and Ovarian Carcinogenesis: Impact on Risk, Prognosis and Therapy Outcome

Tomášová

Čumová

Šeborová

et al. 2020

Cancers

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There is ample evidence for the essential involvement of DNA repair and DNA damage response in the onset of solid malignancies, including ovarian cancer. Indeed, high-penetrance germline mutations in DNA repair genes are important players in familial cancers: BRCA1, BRCA2 mutations or mismatch repair, and polymerase deficiency in colorectal, breast, and ovarian cancers. Recently, some molecular hallmarks (e.g., TP53, KRAS, BRAF, RAD51C/D or PTEN mutations) of ovarian carcinomas were identified. The manuscript overviews the role of DNA repair machinery in ovarian cancer, its risk, prognosis, and therapy outcome. We have attempted to expose molecular hallmarks of ovarian cancer with a focus on DNA repair system and scrutinized genetic, epigenetic, functional, and protein alterations in individual DNA repair pathways (homologous recombination, non-homologous end-joining, DNA mismatch repair, base- and nucleotide-excision repair, and direct repair). We suggest that lack of knowledge particularly in non-homologous end joining repair pathway and the interplay between DNA repair pathways needs to be confronted. The most important genes of the DNA repair system are emphasized and their targeting in ovarian cancer will deserve further attention. The function of those genes, as well as the functional status of the entire DNA repair pathways, should be investigated in detail in the near future.

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Section: Nucleotide Excision Repairmentioning

confidence: 99%

DNA Repair and Ovarian Carcinogenesis: Impact on Risk, Prognosis and Therapy Outcome

Tomášová

Čumová

Šeborová

et al. 2020

Cancers

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“…Moreover, TIE-1 overexpression was observed in many types of cancer, including gastric- [14,15], colon- [16], and breast-cancer cells [17], but the significance of TIE-1 overexpression in cancer remains unknown. We previously reported that TIE-1 promotes DNA damage repair, thereby rendering ovarian-cancer cells resistant to cisplatin [18]. Therefore, TIE-1 might be a potential target for anticancer treatment.…”

Section: Introductionmentioning

confidence: 99%

Potential of Tyrosine Kinase Receptor TIE-1 as Novel Therapeutic Target in High-PI3K-Expressing Ovarian Cancer

Zhang

Ishibashi

Kitatani

et al. 2020

Cancers

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Tyrosine kinase receptor TIE-1 plays a critical role in angiogenesis and blood-vessel stability. In recent years, increased TIE-1 expression has been observed in many types of cancers; however, the biological significance and underlying mechanisms remain unknown. Thus, in the present study, we investigated the tumor biological functions of TIE-1 in ovarian cancer. The treatment of SKOV3 ovarian-cancer cells with siRNA against TIE-1 decreased the expression of key molecules in the PI3K/Akt signaling pathway, such as p110α and phospho-Akt, suggesting that TIE-1 is related to the PI3K/Akt pathway. Furthermore, the knockdown of TIE-1 significantly decreased cell proliferation in high-PI3K-expressing cell lines (SKOV3, CAOV3) but not low-PI3K-expressing cell lines (TOV112D, A2780). These results suggested that inhibition of TIE-1 decreases cell growth in high-PI3K-expressing cells. Moreover, in low-PI3K-expressing TOV112D ovarian-cancer cells, TIE-1 overexpression induced PI3K upregulation and promoted a PI3K-mediated cell proliferative phenotype. Mechanistically, TIE-1 participates in cell growth and proliferation by regulating the PI3K/Akt signaling pathway. Taken together, our findings strongly implicate TIE-1 as a novel therapeutic target in high-PI3K-expressing ovarian-cancer cells.

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“…Drug resistance is attributed to high mortality in a number of other cancers besides NSCLC, including ovarian, breast, and colorectal cancer [10]. In ovarian cancer, Tie1, which forms part of the tyrosine kinase with immunoglobin and EGF homology domains (TIE) signaling pathway, was found to be involved in platinum-resistance and its high expression was correlated with a signi cantly poor prognosis [11]. Ishibashi et al [11] found that overexpression of Tie1, upregulates nucleotide excision repair to counteract the DNA-adduct damage and subsequent apoptosis caused by cisplatin and other platinum agents.…”

Section: Introductionmentioning

confidence: 99%

“…In ovarian cancer, Tie1, which forms part of the tyrosine kinase with immunoglobin and EGF homology domains (TIE) signaling pathway, was found to be involved in platinum-resistance and its high expression was correlated with a signi cantly poor prognosis [11]. Ishibashi et al [11] found that overexpression of Tie1, upregulates nucleotide excision repair to counteract the DNA-adduct damage and subsequent apoptosis caused by cisplatin and other platinum agents. Tie1 encodes a tyrosine kinase receptor that not only has involvement in drug resistance but may also function in tumorigenesis [12].…”

Section: Introductionmentioning

confidence: 99%

Hypoxia-induced Tie1 Drives Stemness and Cisplatin Resistance in Non-small Cell Lung Carcinoma Cells

Yang

Chen

et al. 2020

Preprint

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Background: Drug resistance and metastasis involving hypoxic tumor environment and persistent stem cell populations are detrimental to the survival of patients with non-small cell lung carcinoma (NSCLC). Tie1 is upregulated in hypoxia and is believed to counteract the effectiveness of platinum agents, by promoting the stemness properties in cells. We have investigated the association of Tie1 with HIF-1α and cisplatin resistance in NSCLC cell lines. Methods: Expression of Tie1 in a pulmonary microvascular endothelial cell line (HPMEC) and in NSCLC cell lines was detected using qRT-PCR and western blot. The effect of Tie1 on cell stemness and migration was examined by sphere-forming assay and transwell assay in NSCLC cells with Tie1 silenced. The regulation of Tie1 by HIF-1α was evaluated by a dual-luciferase reporter assay and chromatinImmune precipitation (ChIP) analysis.Results: We found that hypoxia could induce stemness and cisplatin resistance in vitro. Tie1 was expressed at low levels in NSCLC cells when compared with human pulmonary microvascular endothelial cells, however, its expression was increased by hypoxia. Additionally, Tie1 knockdown could reduce the stemness properties and increase sensitivity to cisplatin in vitro and in a xenograft mouse model. The promoter of Tie1 contains two predicted hypoxia-response elements (HREs). We mutated both HRE sites and conducted chromatin immune-precipitation and promoter luciferase reporter assays and were able to conclude that the induction of Tie1 by hypoxia was HIF-1α-dependent. Conclusions: Our findings indicated that Tie1 is upregulated in a hypoxic environment by HIF-1α and contributes to tumorigenesis and cisplatin resistance through the promotion of stemness in NSCLC cells.

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Tyrosine kinase receptor TIE-1 mediates platinum resistance by promoting nucleotide excision repair in ovarian cancer

Cited by 23 publications

References 38 publications

DNA Repair and Ovarian Carcinogenesis: Impact on Risk, Prognosis and Therapy Outcome

DNA Repair and Ovarian Carcinogenesis: Impact on Risk, Prognosis and Therapy Outcome

Potential of Tyrosine Kinase Receptor TIE-1 as Novel Therapeutic Target in High-PI3K-Expressing Ovarian Cancer

Hypoxia-induced Tie1 Drives Stemness and Cisplatin Resistance in Non-small Cell Lung Carcinoma Cells

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