Effect of silencing of mediator of <scp>DNA</scp> damage checkpoint protein 1 on the growth of oral squamous cell carcinoma in vitro and in vivo

Zhang, Xiaoying; Hu, Fengling; Liu, Liuhui; Xu, Bin

doi:10.1111/eos.12662

Cited by 6 publications

(2 citation statements)

References 22 publications

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“…Transwell assays were performed as previously described [ 27 ]. Briefly, the Transwell chambers were uncoated for evaluation of cell migration capabilities, or pre-coated with 80 μL Matrigel (BD, USA) for 30 min for evaluation of cell invasion capabilities.…”

Section: Methodsmentioning

confidence: 99%

MicroRNA-135b-5p regulates trophoblast cell function by targeting phosphoinositide-3-kinase regulatory subunit 2 in preeclampsia

Zhang

Zhang²

2022

Bioengineered

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The level of miR‑135b-5p is lower in patients with preeclampsia (PE) superimposed on chronic hypertension than in healthy controls. However, the function of miR‑135b-5p in PE progression remains unknown. In the present study, we investigated the role of miR‑135b-5p in PE development and its possible mechanism for the first time. HTR8/SVneo cells (trophoblast cell line) were exposed to hypoxia/reoxygenation (H/R) to mimic PE in vitro . Hypoxia-inducible factor-1α (HIF-1α), forkhead box O3A (FOXO3a), and miR-135b-5p levels were measured using Real-time PCR. Cell proliferation, apoptosis and migration/invasion were evaluated using the Cell Counting Kit-8 (CCK-8), flow cytometry and transwell assays, respectively. Real-time PCR and Western blotting were performed to determine the levels of several pro- and anti-angiogenic factors. The binding of miR-135b-5p to the PIK3R2-3’ untranslated region (3ʹUTR) was confirmed by bioinformatics analysis and a dual-luciferase reporter assay. H/R exposure greatly upregulated HIF-1α, FOXO3a, and PIK3R2 levels, while downregulating miR-135b-5p levels in HTR8/SVneo cells. H/R exposure resulted in the inhibition of proliferation, migration, invasion, angiogenesis, and the induction of apoptosis. MiR-135b-5p overexpression reversed the effects of H/R on trophoblast cell function, while miR-135b-5p knockdown enhanced the effects. PIK3R2 knockdown had similar effects as miR-135b-5p overexpression on proliferation, apoptosis and angiogenesis. The effect of miR-135b-5p overexpression on H/R-exposed cells was enhanced by PIK3R2 knockdown. MiR-135b-5p downregulated PIK3R2 expression by pairing with its 3ʹUTR. Therefore, miR-135b-5p may regulate trophoblast function by targeting PIK3R2 in PE and could serve as a novel therapeutic target for PE.

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Section: Methodsmentioning

confidence: 99%

MicroRNA-135b-5p regulates trophoblast cell function by targeting phosphoinositide-3-kinase regulatory subunit 2 in preeclampsia

Zhang

Zhang²

2022

Bioengineered

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“…Studies have shown that the expression of Mre11 in oral cancer tissues is significantly higher than that in adjacent noncancerous oral tissues and that oral cancers with high MRE11 expression have reduced OS and progression-free survival (42). In addition, the mediator of DNA damage checkpoint protein 1 (MDC1) is associated with the recruitment of DNA damage repair proteins to the site of DSBs (65). Clinical studies have shown that in OSCC (100 patients), nuclear and cytoplasmic MDC1 protein expression levels were 85% and 92%, respectively.…”

Section: Dna Damage Repair In Hnsccmentioning

confidence: 99%

Targeting DNA damage response as a potential therapeutic strategy for head and neck squamous cell carcinoma

Lei

He²,

Jiang³

et al. 2022

Front. Oncol.

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Cells experience both endogenous and exogenous DNA damage daily. To maintain genome integrity and suppress tumorigenesis, individuals have evolutionarily acquired a series of repair functions, termed DNA damage response (DDR), to repair DNA damage and ensure the accurate transmission of genetic information. Defects in DNA damage repair pathways may lead to various diseases, including tumors. Accumulating evidence suggests that alterations in DDR-related genes, such as somatic or germline mutations, single nucleotide polymorphisms (SNPs), and promoter methylation, are closely related to the occurrence, development, and treatment of head and neck squamous cell carcinoma (HNSCC). Despite recent advances in surgery combined with radiotherapy, chemotherapy, or immunotherapy, there has been no substantial improvement in the survival rate of patients with HNSCC. Therefore, targeting DNA repair pathways may be a promising treatment for HNSCC. In this review, we summarized the sources of DNA damage and DNA damage repair pathways. Further, the role of DNA damage repair pathways in the development of HNSCC and the application of small molecule inhibitors targeting these pathways in the treatment of HNSCC were focused.

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Modifying effects of nerolidol on cell surface glycoconjugates and suppressed inflammation during DMBA-induced oral carcinogenesis: An in vivo and in silico

et al. 2022

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Effect of silencing of mediator of DNA damage checkpoint protein 1 on the growth of oral squamous cell carcinoma in vitro and in vivo

Cited by 6 publications

References 22 publications

MicroRNA-135b-5p regulates trophoblast cell function by targeting phosphoinositide-3-kinase regulatory subunit 2 in preeclampsia

MicroRNA-135b-5p regulates trophoblast cell function by targeting phosphoinositide-3-kinase regulatory subunit 2 in preeclampsia

Targeting DNA damage response as a potential therapeutic strategy for head and neck squamous cell carcinoma

Modifying effects of nerolidol on cell surface glycoconjugates and suppressed inflammation during DMBA-induced oral carcinogenesis: An in vivo and in silico

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