Nitidine chloride inhibits proliferation and induces apoptosis in colorectal cancer cells by suppressing the ERK signaling pathway

Zhai, Hao‐Ran; Hu, Sanyuan; Liu, Tongxiang; Wang, Feng; Wang, Xixun; Wu, Guoqing; Zhang, Yifei; Sui, Mao; Liu, Huantao; Jiang, Lixin

doi:10.3892/mmr.2016.4827

Cited by 32 publications

(32 citation statements)

References 30 publications

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“…NC was identified to impede the proliferation of CRC cells and induce apoptosis [56]. NC treatment in CRC cells promoted the protein level of Bax, p53, cleaved caspase-3 and -9, and decreased Bcl-2 level and reduced the phosphorylation of ERK, which could lead to cell proliferation inhibition and apoptosis [56]. Elevation of STAT3 expression is observed and associated with metastasis in GC [57].…”

Section: Other Cancersmentioning

confidence: 99%

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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Section: Other Cancersmentioning

confidence: 99%

Antitumor functions and mechanisms of nitidine chloride in human cancers

Cui¹,

Wu²,

Cao³

et al. 2020

J. Cancer

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“…Many efforts have been devoted to study the CRC malignancy in terms of cell proliferation, apoptosis, migration and invasion. Zhai et al, found that nitidine chloride, a natural bioactive molecule, could induce apoptosis and inhibit proliferation in CRC cells via the signal‐regulated kinase (ERK) signalling pathway. The ERK‐dependent migration and invasion of CRC cells were demonstrated to be associated with matrix metalloproteinase 9 (MMP9) upregulation and epidermal growth factor receptor (EGFR) activation .…”

Section: Introductionmentioning

confidence: 99%

SPNS2 promotes the malignancy of colorectal cancer cells via regulating Akt and ERK pathway

Jiang

Wang

et al. 2019

Clin Exp Pharma Physio

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Colorectal cancer (CRC) is a prevalent malignant tumour that causes considerable cancer‐related deaths globally. The sphingolipid transporter 2 (SPNS2), a sphingosine‐1‐phosphate (S1P) transporter, modulates multiple biological events including malignancy of cancer cells. In this study, the effects of SPNS2 on CRC progression were studied. We found that SPNS2 expression was significantly upregulated in CRC tissues compared to that in adjacent non‐tumour tissues. To assess the role of SPNS2 in CRC cells, we performed loss‐ and gain‐of‐function experiments in SW480 and HCT116 cells, respectively. The results demonstrated that SPNS2 promoted proliferation, migration and invasion, and inhibited apoptosis in CRC cells. Additionally, SPNS2 enhanced the release of intracellular S1P, and increased S1P receptor 1 (S1PR1) and S1PR3 expression. Moreover, SPNS2 activated the Akt and ERK pathways, and the biological behaviours of SPNS2 were attenuated by Akt or ERK inhibitor in HCT116 cells. In conclusion, our results demonstrated that SPNS2 promoted proliferation, migration and invasion, and inhibited apoptosis by regulating S1P/S1PR1/3 axis and activating Akt and ERK pathway in CRC cells.

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“…The activity of Akt is also regulated by casein kinase 2 (CK2) inhibitor (12). Mitogen-activated protein kinase (MAPK) signalling pathways relay and integrate signals from a wide range of stimuli and control cellular proliferation, cell cycle and apoptosis (13)(14)(15)(16)(17).…”

Section: Introductionmentioning

confidence: 99%

Quinalizarin exerts an anti-tumour effect on lung cancer A549 cells by modulating the Akt, MAPK, STAT3 and p53 signalling pathways

Liu

Luo

et al. 2017

Mol Med Report

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Quinalizarin may be a potential chemical agent for cancer therapy, as it exerts anti‑tumour effects against a variety of different types of cancer. However, the underlying regulatory mechanism and signalling pathways of quinalizarin in lung cancer cells remains unknown. The present study sought to investigate the effects of quinalizarin on proliferation, apoptosis and reactive oxygen species (ROS) generation in lung cancer. MTT assays were used to evaluate the effects of quinalizarin on the viability of lung cancer A549, NCI‑H460 and NCI‑H23 cells. Flow cytometry was employed to evaluate the effects of quinalizarin on the cell cycle, apoptosis and ROS generation in A549 cells. Western blotting was performed to detect cell cycle and apoptosis‑associated protein expression levels in A549 cells. Quinalizarin inhibited A549, NCI‑H460 and NCI‑H23 cell proliferation and induced A549 cell cycle arrest at the G0/G1 phase. Quinalizarin induced apoptosis by upregulating the expression of B‑cell lymphoma 2 (Bcl‑2)‑associated agonist of cell death, cleaved‑caspase‑3 and cleaved‑poly (adenosine diphosphate‑ribose) polymerase, and downregulating the expression of Bcl‑2. Furthermore, quinalizarin activated mitogen‑activated protein kinase (MAPK) and p53, and inhibited the protein kinase B and signal transducer and activator of transcription‑3 (STAT3) signalling pathways. In addition, quinalizarin increased ROS generation. The ROS scavenger N‑acetyl‑L‑cysteine restored quinalizarin‑induced cell apoptosis, and inactivated the MAPK and STAT3 signalling pathways. The results of the present study demonstrated that quinalizarin induces G0/G1 phase cell cycle arrest and apoptosis via ROS mediated‑MAPK and STAT3 signalling pathways.

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Nitidine chloride inhibits proliferation and induces apoptosis in colorectal cancer cells by suppressing the ERK signaling pathway

Cited by 32 publications

References 30 publications

Antitumor functions and mechanisms of nitidine chloride in human cancers

Antitumor functions and mechanisms of nitidine chloride in human cancers

SPNS2 promotes the malignancy of colorectal cancer cells via regulating Akt and ERK pathway

Quinalizarin exerts an anti-tumour effect on lung cancer A549 cells by modulating the Akt, MAPK, STAT3 and p53 signalling pathways

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