Effects of artemisinin and its derivatives on growth inhibition and apoptosis of oral cancer cells

Nam, Woong; Tak, Jungae; Ryu, Ju Kyoung; Jung, Mankil; Yook, Jong In; Kim, Hyung Jun; Cha, In‐Ho

doi:10.1002/hed.20524

Cited by 127 publications

(95 citation statements)

References 19 publications

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“…DHA, a semi-synthetic derivative of the herbal antimalarial drug artemisinin, can obviously inhibit the growth of a variety of cancer cells, including breast cancer, leukemia, cervical cancer, ovarian cancer, lung cancer, gliomaand oral cancer (Jiao et al, 2007;Nam et al, 2007;Mu et al, 2008;Chen et al, 2009;Handrick et al, 2010). Our studies indicated that DHA inhibited the growth of A549 lung cancer cells.…”

Section: Discussionmentioning

confidence: 60%

“…DHA is shown to have anticancer effects in a wide variety of cancer models in vitro and in vivo (Jiao et al, 2007;Sun et al, 2014). Many studies have shown that DHA inhibits cell proliferation, and induces apoptosis in various human cancer cell lines via down-regulating cyclin (D1, E), Bcl-2, Bcl-xL, caspase-3, caspase-9 and VEGF, while up-regulating P21, P27 and Bax (Nam et al, 2007;Mu et al, 2008;Chen et al, 2009;Chen et al, 2010;Handrick et al, 2010). Therefore, the targeted efficacy of DHA on the TCTP expression of lung cancer cell was explored in the study.…”

Section: Targeted Efficacy Of Dihydroartemisinin For Translationally mentioning

confidence: 99%

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Targeted Efficacy of Dihydroartemisinin for Translationally Controlled Protein Expression in a Lung Cancer Model

Liu

Wu²,

Guo³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Objective: Lung cancer is one of the malignant tumors with greatest morbidity and mortality around the world. The keys to targeted therapy are discovery of lung cancer biomarkers to facilitate improvement of survival and quality of life for the patients with lung cancer. Translationally controlled tumor protein (TCTP) is one of the most overexpressed proteins in human lung cancer cells by comparison to the normal cells, suggesting that it might be a good biomarker for lung cancer. Materials and Methods: In the present study, the targeted efficacy of dihydroartemisinin (DHA) on TCTP expression in the A549 lung cancer cell model was explored. Results and Conclusions: DHA could inhibit A549 lung cancer cell proliferation, and simultaneously up-regulate the expression of TCTP mRNA, but down-regulate its protein expression in A549 cells. In addition, it promoted TCTP protein secretion. Therefore, TCTP might be used as a potential biomarker and therapeutic target for non-small cell lung cancers.

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Section: Discussionmentioning

confidence: 60%

Section: Targeted Efficacy Of Dihydroartemisinin For Translationally mentioning

confidence: 99%

Targeted Efficacy of Dihydroartemisinin for Translationally Controlled Protein Expression in a Lung Cancer Model

Liu

Wu²,

Guo³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…The presence of activated caspase-3 indicates that apoptosis is at the irreversible stage [20] . Nam et al [21] found that artemisinin can induce apoptosis by up-regulating caspase-3. Our study also showed that the activity of caspase-3 in pancreatic acinar cells was obviously elevated after artemisinin was added, indicating that artemisinin may promote apoptosis.…”

Section: Research Frontiersmentioning

confidence: 99%

Induction of apoptosis by artemisinin relieving the severity of inflammation in caerulein-induced acute pancreatitis

Zhao

Xue²,

Zheng³

et al. 2007

WJG

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AIM:To observe the apoptosis and oncosis of pancreatic acinar cells and secondary inflammatory reaction in pancreatic tissue from rats with acute pancreatitis (AP), and the influences of artemisinin on them. METHODS: AP was induced by 4 intraperitonealinjections of caerulein at 1 h intervals. To induce apoptosis, solution of artemisinin (50 mg/kg) was given intraperitoneally 1, 12, 24 and 36 h after the last caerulein injection. Histological examination of impairment of pancreatic tissue and detection of serum amylase were performed to evaluate the severity of acute pancreatitis. Apoptosis and oncosis were detected with acridine orange (AO) and ethylene dibromide (EB) staining. Caspase-3 and myeloperoxidase (MPO) activity were measured by colorimetric assay. Nuclear factor-kappa B (NF-κB) activation was detected by flow cytometry. Macrophage inflammatory protein-1α (MIP-1α) protein was measured by Western blot. Interleukin-1β (IL-1β) mRNA was detected by RT-PCR. RESULTS:Addition of artemisinin increased the number of apoptotic cells (11.7% ± 1.4% vs 6.3% ± 0.7%, P < 0.05), while reduced the number of oncotic cells (13.0% ± 2.4% vs 17.5% ± 2.2%, P < 0.05). The activity of caspase-3 speeded up (1.52 ± 0.21 vs 1.03 ± 0.08, P < 0.05), the pancreas pathological impairment was relieved (3.0 ± 0.5 vs 4.0 ± 0.5, P < 0.05) and the level of serum amylase decreased (5642 ± 721 U/dL vs 7821 ± 653 U/dL, P < 0.05). The activation of NF-κB (29% ± 4.1% vs 42% ± 5.8%), MIP-1α protein (3.7 ± 0.5 vs 5.8 ± 0.7), MPO (0.52 ± 0.06 U/g vs 0.68 ± 0.09 U/g), IL-1β mRNA (1.7 ± 0.3 vs 2.4 ± 0.4) in the apoptosis inducing group was obviously decreased (P < 0.05).

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“…Yook (Yonsei University College of Dentistry, Korea) 14) , and cultured in an incubator at 5% CO2 and 37 o C, on T75 flasks using RPMI 1640 medium containing 5% fetal bovine serum (Hyclone, Logan, UT, USA) and 1% penicillin-streptomycin (Lonza, Allendale, NJ, USA).…”

Section: Cell Culturementioning

confidence: 99%

Lysophosphatidic Acid-Induced TWIST1 and Slug Expression in Oral Cancer Cell Invasion

Cho

2017

J Dent Hyg Sci

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Relative to its incidence, oral cancer has serious negative social effects. The exact causes of oral cancer have not been clarified, but many studies have implicated smoking and drinking. However, the fundamental mechanism of oral cancer causation has yet to be elucidated. Lysophosphatidic acid (LPA) augments epithelial mesenchymal transition (EMT) and development of various cancer cells. However, a detailed mechanistic explanation for LPA-induced EMT and the effects of EMT-promoting conditions on oral squamous cell carcinoma development remain elusive. In the present study, a quantitative reverse transcription polymerase chain reaction was used to analyze TWIST1, Slug, E-cadherin, and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) transcript expression. Immunoblotting was used to analyze TWIST1, Slug, E-cadherin, and GAPDH protein expression. siRNAs were used to silence TWIST1 and Slug transcript expression. A matrigel-coated in vitro invasion insert was used to analyze oral cancer cell invasion. The results of the present study show that the expression levels of TWIST1 and Slug, which are EMT factors, were increased by LPA treatment in YD-10B oral squamous cell carcinoma. Conversely, E-cadherin expression was significantly reduced. In addition, transfection of the cells with TWIST1 and Slug siRNA strongly inhibited LPA-induced oral cancer cell invasion. The present study shows that TWIST1 and Slug mediate LPA-induced oral cancer cell EMT and invasiveness. The present study confirmed the mechanism by which LPA promotes oral cancer cell development, with TWIST1 and Slug providing novel biomarkers and promising therapeutic targets for oral cancer cell development.

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Effects of artemisinin and its derivatives on growth inhibition and apoptosis of oral cancer cells

Cited by 127 publications

References 19 publications

Targeted Efficacy of Dihydroartemisinin for Translationally Controlled Protein Expression in a Lung Cancer Model

Targeted Efficacy of Dihydroartemisinin for Translationally Controlled Protein Expression in a Lung Cancer Model

Induction of apoptosis by artemisinin relieving the severity of inflammation in caerulein-induced acute pancreatitis

Lysophosphatidic Acid-Induced TWIST1 and Slug Expression in Oral Cancer Cell Invasion

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