Down-regulation of JMJD5 suppresses metastasis and induces apoptosis in oral squamous cell carcinoma by regulating p53/NF-κB pathway

Yao, Yuan; Zhou, Wenying; He, Rui-Wen

doi:10.1016/j.biopha.2018.07.144

Cited by 34 publications

(35 citation statements)

References 58 publications

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“…Some of the BMI-correlated genes identified in this study have also been reported in different tumors by previous studies. For example, we identified BMI-correlated genes AKAP5 and JMJD5 in CESC, while it was reported that knockdown AKAP5 inhibited ERK1/2 activity and downregulation JMJD5 suppresses oral squamous cell carcinoma metastasis and induces apoptosis via p53/NF-κB pathway [53,54].…”

Section: Discussionmentioning

confidence: 99%

Body mass index-associated molecular characteristics involved in tumor immune and metabolic pathways

Chen

Yao

et al. 2020

Cancer Metab

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Background Overweight or obesity has been evidenced as an important risk factor involved in the incidence, mortality, and therapy response of multiple malignancies. However, the differences between healthy and obesity tumor patients at the molecular and multi-omics levels remain unclear. Methods Our study performed a comprehensive and multidimensional analysis in fourteen tumor types of The Cancer Genome Atlas (TCGA) and found body mass index (BMI)-related genes in multiple tumor types. Furthermore, we compared composite expression between normal, overweight, and obese patients of each immune cell subpopulation and metabolism gene subset. Statistical significance was calculated via the Kruskal-Wallis rank-sum test. Results Our analysis revealed that BMI-related genes are enriched in multiple tumor-related biological pathways involved in intracellular signaling, immune response, and metabolism. We also found the different relationships between BMI and different immune cell infiltration and metabolic pathway activity. Importantly, we found that many clinically actionable genes were BMI-affect genes. Conclusion Overall, our data indicated that BMI-associated molecular characteristics involved in tumor immune and metabolic pathways, which may highlight the clinical importance of considering BMI-associated molecular signatures in cancer precision medicine.

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Section: Discussionmentioning

confidence: 99%

Body mass index-associated molecular characteristics involved in tumor immune and metabolic pathways

Chen

Yao

et al. 2020

Cancer Metab

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“…Bax, a pro‐apoptotic molecule, is the key member of Bcl‐2 family. The activation of Bax stimulates caspase‐3/7 and subsequently promotes the cleavage of PARP, which induces the apoptotic process . Cleaved‐PARP, cleaved‐caspase‐3 and cleaved‐caspase‐7 were applied for diagnosing the apoptosis in colorectal cancer .…”

Section: Discussionmentioning

confidence: 99%

“…The activation of Bax stimulates caspase-3/7 and subsequently promotes the cleavage of PARP, which induces the apoptotic process. 15 Cleaved-PARP, cleavedcaspase-3 and cleaved-caspase-7 were applied for diagnosing the apoptosis in colorectal cancer. 16 Survivin, the member belongs to the apoptosis inhibitor protein family, was reported to be highly related to caspase-3/7 pathway and participate in the modulation of colon cancer.…”

Section: ##mentioning

confidence: 99%

Lobetyolin induces apoptosis of colon cancer cells by inhibiting glutamine metabolism

Tao

Zhang

et al. 2020

J Cellular Molecular Medi

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The purpose of the present study was to evaluate the anti‐cancer property of Lobetyolin on colorectal cancer and explore its potential mechanism. Lobetyolin was incubated with HCT‐116 cells in the absence or presence of ASCT2 inhibitor Benser or p53 inhibitor Pifithrin‐α. The levels of glutamine, glutamic acid, α‐ketoglutarate, ATP and GSH were determined to measure the glutamine metabolism. Annexin V‐FITC/PI staining and TUNEL assay were applied to estimate the apoptotic condition. The levels of ASCT2 were examined by RT‐qPCR, Western blot and immunofluorescence staining. The expressions of cleaved‐caspase‐3, caspase‐3, cleaved‐caspase‐7, caspase‐7, cleaved‐PARP, PARP, p53, p21, bax and survivin were detected using Western blot analysis. As a result, the treatment with Lobetyolin effectively induced apoptosis and glutamine metabolism in HCT‐116 cells through ASCT2 signalling. The inhibition of ASCT2 reduced the glutamine‐related biomarkers and augmented the apoptotic process. We further found that the effect of Lobetyolin on HCT‐116 was related to the expressions of p21 and bax, and transportation of p53 to nucleus. The inhibition of p53 by Pifithrin‐α promoted the inhibitory effect of Lobetyolin on ASCT2‐mediated apoptosis. Lobetyolin also exerted anti‐cancer property in nude mice. In conclusion, the present work suggested that Lobetyolin could induce the apoptosis via the inhibition of ASCT2‐mediated glutamine metabolism, which was possibly governed by p53.

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“…Male SPF BALB/c nude mice aged 4–5 wk (16–20 g, with a SD of 1.23 g) were obtained from Shanghai Sippr‐BK Laboratory Animal (Shanghai, China). Nude mice were randomly divided into the MDC1 interference group (si‐MDC1; n = 6) and the negative‐control group (si‐con; n = 6), and 5 × 10 6 si‐con‐ or si‐MDC1‐transfected Tca‐8113 cells were subcutaneously inoculated into the left flank of each mouse . The long diameter ( a ) and short diameter ( b ) of the tumor that grew in each mouse at the injection site were measured using a Vernier caliper every 2 d. The tumor volume was calculated according to the formula: V = a × b 2 /2, and the tumor growth curve was plotted.…”

Section: Methodsmentioning

confidence: 99%

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

Zhang

Liu

et al. 2019

European J Oral Sciences

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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. Eur J Oral Sci 2019; 127: 494-499. © 2019 Eur J Oral SciMediator of DNA damage checkpoint protein 1 (MDC1) is involved in DNA damage repair and has been linked to tumor invasion, metastasis, and prognosis. This study investigated the effects of MDC1 in oral squamous cell carcinoma (OSCC) in vitro and in vivo. RNA interference-mediated knockdown of MDC1 was performed in two OSCC cell lines (Tca-8113 and KB). Real-time PCR and western blotting were performed to determine expression of mRNA and protein, respectively, of MDC1. Cell viability was assessed using the MTT assay. Colony-formation assays were performed by staining with 0.5% crystal violet. Cell migration and invasion were detected by Transwell assays. The role of MDC1 in OSCC was examined in vivo via injection of Tca-8113 cells transfected with MDC1 small interfering (si)RNA or negative-control siRNA into a mouse xenograft model of OSCC. Our results showed that MDC1 knockdown decreased cell proliferation. Inhibition of MDC1 decreased colony formation of Tca-8113 and KB cells by 62% and 68%, respectively, and MDC1 knockdown reduced the number of migratory and invasive cells compared with the control group. Moreover, the xenograft mouse model of MDC1 knockdown showed reduced tumor growth. Our study suggests that MDC1 plays a role in tumorigenesis and might be a potential target for the treatment of patients with OSCC. Material and methods Cell cultureThe OSCC cell lines Tca-8113 and KB were obtained from the Shanghai Cell Bank of the Chinese Academy of Sciences (Shanghai, China). Both cell lines were authenticated by short tandem repeat analysis and were mycoplasma-free. Tca-8113 and KB cells were inoculated into RPMI-1640 (Gibco, Invitrogen, Paisley, UK) containing

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Down-regulation of JMJD5 suppresses metastasis and induces apoptosis in oral squamous cell carcinoma by regulating p53/NF-κB pathway

Cited by 34 publications

References 58 publications

Body mass index-associated molecular characteristics involved in tumor immune and metabolic pathways

Body mass index-associated molecular characteristics involved in tumor immune and metabolic pathways

Lobetyolin induces apoptosis of colon cancer cells by inhibiting glutamine metabolism

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

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