Grape seed proanthocyanidins inhibit the proliferation, migration and invasion of tongue squamous cell carcinoma cells through suppressing the protein kinase?B/nuclear factor-κB signaling pathway

Yang, Ninggang; Gao, Jing; Cheng, Xin; Hou, Chunmei; Yang, Yuqing; Qiu, Yanxin; Xu, Mengrou; Zhang, Yuan; Huang, Shuangsheng

doi:10.3892/ijmm.2017.3162

Cited by 18 publications

(23 citation statements)

References 42 publications

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“…28 GSPs were reported to significantly suppress the migratory and invasive ability of tongue squamous cell carcinoma (TSCC) cells through blocking the secretion of matrix metalloproteinases. 29 Similarly, the experiment of in vivo bioluminescence imaging showed that dietary administration of GSPs could suppress the migration of intravenously injected melanoma cells through the activation of β-catenin and its downstream targets in the lungs of immune-compromised nude mice. 30 In our results, the reduction of SiHa and HeLa cells migration and invasion in our study indicated that the treatment of PC could also markedly inhibit the metastasis progression of CC by controlling tumor cell migration and invasion.…”

Section: Discussionmentioning

confidence: 99%

<p>Procyanidin Compound (PC) Suppresses Lipopolysaccharide-Induced Cervical Cancer Cell Proliferation Through Blocking the TLR4/NF-κB Pathway</p>

Yang

Fang

et al. 2020

CMAR

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Evidence suggested that procyanidin compound (PC) could inhibit the progression of cervical cancer (CC); however, the mechanism still remains unclear. We aimed to study the potential mechanism of PC acting on CC cells. Patients and Methods: After a 24 hr incubation of lipopolysaccharide (LPS) (1 μg/mL), human CC SiHa and HeLa cells were cultured with various concentrations (20, 40, and 80 μg/ mL) of PC for 24 hrs, then the cell viability was detected using Cell Counting Kit-8 (CCK-8). The migration and invasion abilities were assessed by scratch and Transwell assays. Apoptosis and cell cycle were detected using flow cytometry. Real-time quantitative PCR (RT-qPCR) and Western blot were used for expression analysis of the inflammatory cytokines. The pathway components were measured to evaluate the involvement of toll-like receptor 4/nuclear factor kappa-light-chain-enhancer of activated B cells (TLR4/NF-κB) pathway. Results: PC inhibited the LPS-primed cell viability in a dose-dependent manner. After PC treatment, cell migration and invasion were inhibited, cell number at the G2/M phase was increased. The CC cell apoptosis was triggered through upregulating levels of cleaved caspase-3 and Bax and downregulating the level of B-cell lymphoma 2 protein. A significant reduction was shown in the levels of interleukin (IL)-6, IL-1β and tumor necrosis factor (TNF)-α. Furthermore, a remarkable reduction in the ratio of TLR4 and the p-P65/t-P65 and in the progression of P65 translocation into the nucleus was observed. Conclusion: Our results revealed that the inhibitory effect of PC on CC cell proliferation relies on the induction of apoptosis and inhibition of inflammatory cytokines.

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Section: Discussionmentioning

confidence: 99%

<p>Procyanidin Compound (PC) Suppresses Lipopolysaccharide-Induced Cervical Cancer Cell Proliferation Through Blocking the TLR4/NF-κB Pathway</p>

Yang

Fang

et al. 2020

CMAR

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“…Tongue squamous cell carcinoma (TSCC), the most common malignant tumor of the oral region, is well known for its high rate of lymph node metastasis and poor prognosis [1,2]. Currently, combination chemotherapy based on cisplatin (cis-diamminedichloroplatinum II, CDDP) is the standard treatment for many types of cancers, including TSCC.…”

Section: Introductionmentioning

confidence: 99%

Plumbagin Enhances the Anticancer Efficacy of Cisplatin by Increasing Intracellular ROS in Human Tongue Squamous Cell Carcinoma

Xue

Pan

Zhou

et al. 2020

Oxidative Medicine and Cellular Longevity

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Cisplatin is widely used in the treatment of tongue squamous cell carcinoma (TSCC), but its clinical efficacy is limited by drug resistance and toxic side effects. Hence, a novel compound capable of enhancing the anticancer effect of cisplatin while reducing the side effects is urgently needed. We have previously shown that plumbagin (PLB), an anticancer phytochemical, is able to inhibit the growth of TSCC in vitro and in vivo. The objective of this study was to investigate the effect of PLB in reversing the resistance of TSCC to cisplatin as well as its molecular mechanisms. Here, we found that PLB enhances cisplatin-induced cytotoxicity, apoptosis, and autophagy in CAL27 and cisplatin-resistant CAL27/CDDP cells. PLB could inhibit the viability and growth of TSCC cells by increasing the production of intracellular reactive oxygen species (ROS). In addition, the combination treatment of PLB and cisplatin resulted in a synergistic inhibition of TSCC viability, apoptosis, and autophagy by increasing intracellular ROS, which may be achieved by activating JNK and inhibiting AKT/mTOR signaling pathways. Finally, the synergistic treatment was also demonstrated in vivo. Therefore, PLB combined with cisplatin is a potential therapeutic strategy against therapy TSCC cisplatin resistance.

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“…Zhao et al (66) reported that c-MYC is likely to drive TSCC progression while Huang et al (67) demonstrated that Iroquois homeobox gene 5 can promote the aggressiveness of TSCC cells by activating the NF-κB signaling pathway, leading to an increase in the nuclear p65 levels and IκBα degradation. In addition, grape seed proanthocyanidin markedly repressed the activity of NF-κB and promoted apoptosis of TSCC cells by regulating the stability and activity of Bax and downgrading the Bcl-2 and Bcl-xL proteins, and additionally suppressed the aggressiveness and metastasis of TSCC cells by restraining the secretion of MMP-2 and MMP-9 in the cells (68). A previous study reported that isobavachalcone may inhibit the expression of the apoptosis-related protein Bcl-2 (69).…”

Section: Discussionmentioning

confidence: 98%

Knockdown of ectodysplasin‑A receptor‑associated adaptor protein exerts a tumor‑suppressive effect in tongue squamous cell carcinoma cells

Bai

Han

et al. 2020

Exp Ther Med

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Tongue squamous cell carcinoma (TSCC) is a common malignancy in oral cancer with a high mortality and morbidity. The ectodysplasin-A receptor-associated adaptor protein (EDARADD) is a death domain-containing adaptor protein that interacts with the TNF family ligand ectodysplasin A receptor. It is known that EDARADD has an effect on the development of ectodermal derivative tissues, such as hair and teeth. EDARADD expression is also associated with the development of melanoma. However, the role of EDARADD in TSCC remains unknown. The aim of the present investigation was to explore whether EDARADD plays a role in the biological function of TSCC. Immunohistochemistry was used to measure the expression of EDARADD in TSCC tissues and adjacent normal tissue. EDARADD was knocked down in a TSCC cell line in vitro using a specific lentivirus. The expression level of the EDARADD gene and the efficacy of gene knockdown were evaluated by reverse transcription-quantitative PCR, while EDARADD protein expression and the expression levels of Bcl-2, MYC and NF-κBp65 were determined by western blotting. Additionally, MTT assays, colony formation assays and apoptosis assays were carried out to examine the effect of EDARADD knockdown on the TSCC cells. A previous study showed that the majority of the TSCC tissues that were tested had high EDARADD expression. The expression of EDARADD both at mRNA and protein levels was significantly lower (P<0.01) after the gene was knocked down in the CAL27 cells compared with the level in control cells. Downregulation of EDARADD expression inhibited colony formation and proliferation and induced apoptosis of CAL27 cells when compared to control cells (P<0.01). Taken together, these results suggested that EDARADD may be actively involved in the progression of TSCC and that EDARADD may be a novel therapeutic target for the treatment of TSCC.

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Grape seed proanthocyanidins inhibit the proliferation, migration and invasion of tongue squamous cell carcinoma cells through suppressing the protein kinase?B/nuclear factor-κB signaling pathway

Cited by 18 publications

References 42 publications

<p>Procyanidin Compound (PC) Suppresses Lipopolysaccharide-Induced Cervical Cancer Cell Proliferation Through Blocking the TLR4/NF-κB Pathway</p>

<p>Procyanidin Compound (PC) Suppresses Lipopolysaccharide-Induced Cervical Cancer Cell Proliferation Through Blocking the TLR4/NF-κB Pathway</p>

Plumbagin Enhances the Anticancer Efficacy of Cisplatin by Increasing Intracellular ROS in Human Tongue Squamous Cell Carcinoma

Knockdown of ectodysplasin‑A receptor‑associated adaptor protein exerts a tumor‑suppressive effect in tongue squamous cell carcinoma cells

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