Sensory acceptable equivalent doses of β-phenylethyl isothiocyanate (PEITC) induce cell cycle arrest and retard the growth of p53 mutated oral cancer in vitro and in vivo

Osteosarcoma is the most common primary malignant bone tumor in children and adolescents. However, the underlying mechanism of osteosarcoma carcinogenesis and progression remains unknown. In the present study, we evaluated the expression profile of miRNAs in osteosarcoma tissues and the adjacent normal tissues. We found that the expression of miR-422a was down-regulated in osteosarcoma tissues and cell lines. In addition, we observed significantly elevated levels of repressive H3K9me3 and H3K27me3 and decreased active H3K4me3 on the promote region of miR-422a in osteosarcoma cells and clinical samples. Furthermore, up-regulation of miR-422a exhibited both in vitro and in vivo anti-tumor effects by inhibiting osteosarcoma cell growth and inducing apoptosis and cell cycle arrest. We also found that miR-422a targeted BCL2L2 and KRAS and negatively regulated their protein expression. Furthermore, restoration of miR-422a and knockdown of BCL2L2 and KRAS promoted apoptosis and induce cell cycle arrest in osteosarcoma cells. Taken together, the present study demonstrates that miR-422a may serve as a tumor suppressor in osteosarcoma via inhibiting BCL2L2 and KRAS translation both in vitro and in vivo. Therefore, miR-422a could be developed as a novel therapeutic target in osteosarcoma.

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Taiwanin E Induces Cell Cycle Arrest and Apoptosis in Arecoline/4-NQO-Induced Oral Cancer Cells Through Modulation of the ERK Signaling Pathway

Frontiers in Oncology ◽

10.3389/fonc.2019.01309 ◽

2019 ◽

Vol 9 ◽

Cited By ~ 1

Author(s):

Shih-Hao Wang ◽

Hsi-Chin Wu ◽

Khan Farheen Badrealam ◽

Yueh-Hsiung Kuo ◽

Yun-Peng Chao ◽

...

Keyword(s):

Cell Cycle ◽

Oral Cancer ◽

Cell Cycle Arrest ◽

Cancer Cells ◽

Signaling Pathway ◽

Erk Signaling ◽

Cycle Arrest ◽

Oral Cancer Cells

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A Marine Alkaloid, Ascomylactam A, Suppresses Lung Tumorigenesis via Inducing Cell Cycle G1/S Arrest through ROS/Akt/Rb Pathway

Marine Drugs ◽

10.3390/md18100494 ◽

2020 ◽

Vol 18 (10) ◽

pp. 494

Author(s):

Lan Wang ◽

Yun Huang ◽

Cui-hong Huang ◽

Jian-chen Yu ◽

Ying-chun Zheng ◽

...

Keyword(s):

Lung Cancer ◽

Cell Cycle ◽

Cell Cycle Arrest ◽

Molecular Mechanisms ◽

Soft Agar ◽

Ros Generation ◽

Induce Cell Cycle Arrest ◽

Cycle Arrest

Ascomylactam A was reported for the first time as a new 13-membered-ring macrocyclic alkaloid in 2019 from the mangrove endophytic fungus Didymella sp. CYSK-4 from the South China Sea. The aim of our study was to delineate the effects of ascomylactam A (AsA) on lung cancer cells and explore the antitumor molecular mechanisms underlying of AsA. In vitro, AsA markedly inhibited the cell proliferation with half-maximal inhibitory concentration (IC50) values from 4 to 8 μM on six lung cancer cell lines, respectively. In vivo, AsA suppressed the tumor growth of A549, NCI-H460 and NCI-H1975 xenografts significantly in mice. Furthermore, by analyses of the soft agar colony formation, 5-ethynyl-20-deoxyuridine (EdU) assay, reactive oxygen species (ROS) imaging, flow cytometry and Western blotting, AsA demonstrated the ability to induce cell cycle arrest in G1 and G1/S phases by increasing ROS generation and decreasing of Akt activity. Conversely, ROS inhibitors and overexpression of Akt could decrease cell growth inhibition and cell cycle arrest induced by AsA. Therefore, we believe that AsA blocks the cell cycle via an ROS-dependent Akt/Cyclin D1/Rb signaling pathway, which consequently leads to the observed antitumor effect both in vitro and in vivo. Our results suggest a novel leading compound for antitumor drug development.

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Berberine induces cell cycle arrest and apoptosis in human HSC‐3 oral cancer cells

The FASEB Journal ◽

10.1096/fasebj.21.6.a1189-c ◽

2007 ◽

Vol 21 (6) ◽

Author(s):

Chin‐Chung Lin ◽

Jiung‐Long Yang ◽

Chi‐Cheng Lu ◽

Jing‐Gung Chung

Keyword(s):

Cell Cycle ◽

Oral Cancer ◽

Cell Cycle Arrest ◽

Cancer Cells ◽

Cycle Arrest ◽

Oral Cancer Cells

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The Novel Herbal Cocktail AGA Alleviates Oral Cancer through Inducing Apoptosis, Inhibited Migration and Promotion of Cell Cycle Arrest at SubG1 Phase

Cancers ◽

10.3390/cancers12113214 ◽

2020 ◽

Vol 12 (11) ◽

pp. 3214

Author(s):

Jui-Hua Lu ◽

Yen-Ru Chou ◽

Yue-Hua Deng ◽

Mao-Suan Huang ◽

Shaw-Ting Chien ◽

...

Keyword(s):

Cell Cycle ◽

Oral Cancer ◽

Cell Cycle Arrest ◽

Cancer Cells ◽

Dependent Manner ◽

Cell Cycle Regulators ◽

Inhibitory Protein ◽

Migration Ability ◽

Cycle Arrest

Traditional Chinese medicines Antler’s extract (A) and Ganoderma lucidum (G) and Antrodia Camphorata (A) have been known to individually contain a plethora of bioactive factors including triterpenoids, polysaccharides etc., exerting various curative impacts such as anti-inflammatory, anti-oxidative, anti-atherosclerotic and anti-viral activities. However, their combinatorial therapeutic efficacy for oral cancer has not been investigated. Hence, we synthesized a robust cocktail called AGA and investigated its anti-oral cancer potential in vitro and in vivo. An MTT assay revealed the IC50 of AGA to be about 15 mg at 72 h. Therefore, 10 mg and 20 mg doses were selected to study the effect of AGA. The AGA significantly inhibited proliferation of oral cancer cells (HSC3, SAS, and OECM-1) in a dose- and time-dependent manner. AGA retarded cell cycle regulators (CDK4, CDK6, cyclin A, B1, D1 and E2) and apoptosis inhibitory protein Bcl-2, but enhanced pro-apoptotic protein Bax and a higher percentage of cells in Sub-G1 phase. Mechanistically, AGA suppressed all EMT markers; consequently, it decreased the migration ability of cancer cells. AGA significantly reduced xenograft tumor growth in nude mice with no adverse events in liver and renal toxicity. Conclusively, AGA strongly inhibited oral cancer through inducing apoptosis and inhibiting the migration and promotion of cell cycle arrest at subG1 phase, which may be mediated primarily via cocktail-contained triterpenoids and polysaccharides.

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