Nitidine chloride inhibits renal cancer cell metastasis via suppressing AKT signaling pathway

Fang, Zhiqing; Tang, Yongxin; Jiao, Wei; Zeng, Xing; Guo, Zhaoxin; Wang, Weichang; Shi, Benkang; Xu, Zhonghua; Liu, Zhaoxu

doi:10.1016/j.fct.2013.07.062

Cited by 38 publications

(40 citation statements)

References 30 publications

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“…Previously, it had been demonstrated that AKT signaling was related not only to the disease development, such as in cancer, (Testa and Bellacosa, ) but also to the response of a tumor to cancer treatment (Lim et al , ). Moreover, therapies that down‐regulate phosphorylated AKT as a novel therapeutic target may be useful in the treatment of a broad range of human cancers (Fang et al , ; Fresno Vara et al , ). Therefore, we investigated the effect of evodiamine on AKT phosphorylation status.…”

Section: Discussionmentioning

confidence: 99%

In Vitro Assessment of the Anticancer Potential of Evodiamine in Human Oral Cancer Cell Lines

Sachita

Kim

et al. 2015

Phytotherapy Research

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Evodiamine, a bioactive alkaloid, has been regarded as having antioxidant, antiinflammatory, and anticancer properties. In the present study, we explored the effects of evodiamine on cell growth and apoptosis in human oral cancer cell lines. Our data revealed that evodiamine significantly inhibited the proliferation of human oral cancer cells and resulted in the cleavages of PARP (poly (ADP-ribose) polymerase) and caspase-3, in addition to causing the typical characteristics of apoptosis. Evodiamine also increased Bax protein levels and caused translocation of Bax into mitochondria and Bax oligomerization. In addition, evodiamine decreased expression of myeloid cell leukemia (Mcl-1) at the transcriptional modification, and knockdown of Mcl-1 clearly resulted in an increase in expression of Bax and active Bax, resulting in induction of apoptosis. Evodiamine reduced expression of phosphorylated AKT, and LY294002 potentiated evodiamine-induced apoptosis by regulating Mcl-1 protein. Our results suggest that evodiamine induces apoptosis in human oral cancer cells through the AKT pathway. These findings provide a rationale for its clinical application in the treatment of oral cancer.

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Section: Discussionmentioning

confidence: 99%

In Vitro Assessment of the Anticancer Potential of Evodiamine in Human Oral Cancer Cell Lines

Sachita

Kim

et al. 2015

Phytotherapy Research

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“…The higher expression of pAkt is exhibited in RCC, especially in later and metastatic RCC [41,42]. One study has shown that NC attenuated the cell invasion and metastasis of RCC cells through inhibition of Akt signaling pathway and MMP-2 and MMP-9 [43]. This group further found that NC inhibited phosphorylation of ERK and Akt, upregulated the protein level of p53, Bax, cleavage caspase-3 and PARP and downregulated Bcl-2 in RCC cells [44].…”

Section: Renal Cancermentioning

confidence: 95%

Antitumor functions and mechanisms of nitidine chloride in human cancers

Cui¹,

Wu²,

Cao³

et al. 2020

J. Cancer

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Nitidine chloride (NC), a quaternary ammonium alkaloid, exhibits multiple biological activities, including antimalarial, antifungal, and antiangiogenesis. Recently, NC has been characterized to perform antitumor activity in a variety of malignancies. NC has been identified to suppress cell proliferation, stimulate apoptosis, and induce cell cycle arrest, retard migration, invasion and metastasis. Moreover, NC is reported to sensitize cancer cells to chemotherapeutic drugs. In this review article, we describe the functions of NC in human cancers and discuss the molecular insight into NC-involved antitumor feature. This review article will stimulate the deeper investigation for using NC as a potent agent for the management of cancer patients.

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“…Extensive reports have demonstrated that NC has anti-oxidant, anti-inflammatory, anti-fungal and anti-HIV functions (2,3). Recently, studies have focused on its antitumor activity in various types of cancers, such as hepatocellular carcinoma (4), gastric (5), breast (6,7), renal (8,9), nasopharyngeal carcinoma (10) and chronic myeloid leukemia (CML) (11). NC have showed activity for inhibiting proliferation and induces apoptosis of hepatocellular carcinoma, gastric, breast and renal cancer (4,5,7,8).…”

Section: Introductionmentioning

confidence: 99%

“…NC have showed activity for inhibiting proliferation and induces apoptosis of hepatocellular carcinoma, gastric, breast and renal cancer (4,5,7,8). Moreover, NC was also shown to suppress invasion and metastasis of breast cancer by suppressing c-Src/FAK associated signaling pathway and renal cancer via Akt pathway (6,9). NC has also been demonstrated to be a powerful chemosensitizer for breast cancers (7).…”

Section: Introductionmentioning

confidence: 99%

Nitidine chloride suppresses epithelial-to-mesenchymal transition in osteosarcoma cell migration and invasion through Akt/GSK-3β/Snail signaling pathway

Cheng¹,

Guo²,

Yang³

et al. 2016

Oncology Reports

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Metastasis is the main cause of death in osteosarcoma. Targeting the process of metastasis is a main strategy for osteosarcoma therapy. As a traditional Chinese medicine, Zanthoxylum nitidum (Roxb) has been applied to treat various diseases, including cancer. However, no evidence has been shown on the anti-metastasis effect of nitidine chloride (NC) that was extracted from Zanthoxylum nitidum (Roxb) on osteosarcoma cells, or its underling mechanisms. In the present study, we aimed to demonstrate the role of NC on the migration and invasion of osteosarcoma cells. Viability and proliferation of osteosarcoma cells were examined by MTT assay. Then, by appling scratch wound healing assay and Transwell assays, we evaluated migratory and invasive ability of the cells, respectively. Moreover, the expression of epithelial-to-mesenchymal transition (EMT) markers were determined after treatment with NC. Furthermore, the expression of Akt, GSK-3β and Snail were detected by western blot analysis. In addition, the GSK-3β activity was examined by GSK-3β kinase assay. Finally, an inhibitor of GSK-3β, lithium chloride (LiCl) was applied to testify the effect of NC on the expression of EMT markers and Snail. We found that the proliferative, migratory and invasive ability of the U2OS osteosarcoma cells were all suppressed when treated with NC. NC increased the expression of E-cadherin and decreased the expression of N-cadherin, vimentin and fibronectin in a dose-dependent manner. NC also exerted its ability to suppress the phosphorylation of Akt and GSK-3β so as to activate GSK-3β. Then, by using an GSK-3β inhibitor, LiCl, we revealed the effect of GSK-3β in the expression of EMT markers. The expression of Snail was inhibited when treated with NC and LiCl also reversed the NC-inhibited Snail expression. Taken together, these results revealed that NC suppressed EMT and decreased the invasive ability of osteosarcoma cells via the Akt/GSK-3β/snail signaling pathway.

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Nitidine chloride inhibits renal cancer cell metastasis via suppressing AKT signaling pathway

Cited by 38 publications

References 30 publications

In Vitro Assessment of the Anticancer Potential of Evodiamine in Human Oral Cancer Cell Lines

In Vitro Assessment of the Anticancer Potential of Evodiamine in Human Oral Cancer Cell Lines

Antitumor functions and mechanisms of nitidine chloride in human cancers

Nitidine chloride suppresses epithelial-to-mesenchymal transition in osteosarcoma cell migration and invasion through Akt/GSK-3β/Snail signaling pathway

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