Osthole inhibits the PI3K/AKT signaling pathway via activation of PTEN and induces cell cycle arrest and apoptosis in esophageal squamous cell carcinoma

Zhu, Xinbing; Li, Zhengzheng; Li, Tongtong; Long, Fei; Lv, Yuesheng; Liu, Lei; Li, Xuefeng; Zhan, Qimin

doi:10.1016/j.biopha.2018.03.106

Cited by 50 publications

(35 citation statements)

References 39 publications

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“…The PI3K/Akt signaling pathway serves a role in cell growth and proliferation, and has been observed to be dysregulated in various cancer types ( 47 ). A previous study demonstrated that the PI3K/Akt signaling pathway is inactivated, whereas osthole promotes the apoptosis of esophageal squamous cell carcinoma ( 48 ). Furthermore, repression of the PI3K/Akt signaling pathway inhibits cell viability and may enhance the apoptosis of PCa ( 49 ), indicating the role of the PI3K/Akt signaling pathway during tumor progression.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of anti-silencing function 1B histone chaperone induces cell apoptosis via repressing PI3K/Akt pathway in prostate cancer

et al. 2018

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Prostate cancer (PCa) is one of the most common malignancies among males worldwide. Anti-silencing function 1B histone chaperone (ASF1B) has been reported to be involved in PCa. The present study aimed to investigate the role and molecular mechanism of ASF1B in PCa. Data of genes were obtained from The Cancer Genome Atlas data- base. The core gene was identified using the DAVID website. Cell viability and colony formation were detected using a cell counting kit-8 assay and crystal violet staining, respectively. Cell cycle distribution and apoptosis were assessed using flow cytometry analysis. The corresponding factors were analyzed by reverse transcription-quantitative polymerase chain reaction and western blotting. It was demonstrated that ASF1B was highly expressed in the PCa tissues and cells compared with the non-PCa tissues and cells, respectively. While siRNA-ASF1B significantly reduced the viability and colony formation, it promoted apoptosis, G1 phase cell cycle arrest of LNCap as well as C4-2 cells. siRNA-ASF1B was revealed to significantly reduce the level of B-cell lymphoma-2 and cyclin D1, and enhance the expression levels of p53, caspase-3 and Bcl-2 associated X protein. Furthermore, the phosphorylation levels of phosphatidylinositol 3 kinase (PI3K) and protein kinase B (Akt) were significantly decreased in the siRNA-ASF1B group compared with the mock group. In summary, the present study demonstrated that silencing of ASF1B suppressed the proliferation, and promoted apoptosis and cell cycle arrest of PCa cells. Inhibition of the PI3K/Akt signaling pathway was pertinent to the role of si-ASF1B. This phenomenon suggests that the downregulation of ASF1B may aid in inhibiting the progression of PCa.

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Section: Discussionmentioning

confidence: 99%

Knockdown of anti-silencing function 1B histone chaperone induces cell apoptosis via repressing PI3K/Akt pathway in prostate cancer

et al. 2018

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“…Besides, osthole could also influence the cell growth circle to induce apoptosis at the G2/M phase via the caspase signaling pathway [188]. Osthole suppressed the clonogenicity of esophageal cell carcinomas (ESCC) cells such as KYSE150 and KYSE410 cells in a dose-dependent manner, plus, it was also noticed that osthole's inhibitory effect against ESCC cells was related to the build-up of cell cycle progression at G2/M phase and apoptosis induction with the activation of caspase-dependent pathway, the P13K/AKT (p-AKT) signaling pathway through the activation of PTEN which was responsible for P13K/AKT pathway negative regulation and cell growth inhibition [189]. For pancreatic cancer, osthole could inhibit pancreatic cancer progression, reduce tumor weight, suppress proliferation, migration, and cause apoptosis of pancreatic 02 cells.…”

Section: Digestive System Cancermentioning

confidence: 98%

“…In vitro [176] Anti-osteoporosis effect Osthole 1 × 10 −4 , 1 × 10 −5 , 1 × 10 −6 , 1 × 10 −7 mol/L. In vitro [177] Anti-osteoporosis effect Osthole 0, 6.25, 12.5, 25, 50 µmol/L In vitro [178] Anti-osteoporosis effect Bone-targeted osthole 10 −4 , 10 −5 , 10 −6 , 10 −7 mmol/L In vitro [179] Anti-osteoporosis effect Osthole 100, 50, 25 µmol/L In vitro [180] Anti-osteoporosis effect Osthole 1 × 10 −5 mol/L In vitro [181] Anti-osteoporosis effect Osthole 10 −5 mol/L In vitro [182] Anti-osteoporosis effect Bone-targeted Osthole 10 −5 mol/L In vitro [183] Anti-osteoporosis effect Osthole 10 −7 , 10 −6 , 10 −5 , and 10 −4 mol/L In vitro [184] Anti-osteoporosis effect Gushudan, a chinese herbal formula with CMC 30 g/kg per day for 12 weeks via oral administration In vivo [185] Bone fracture healing effect Osthole 20 mg/kg for 1, 2, 3 weeks among 3 groups via oral gavage In vivo+ In vitro [186] Anti-osteoporosis effect Total flavonoids 5 mL/kg per day for 90 days In vivo [187] Anti-osteoporosis effect Osthole 10 mg/kg per day for 5 days via subcutaneous injection In vivo [188] Anti-periodontitis effect Osthole 10 −4 , 10 −5 , 10 −6 , and 10 −7 m/L for 3 days In vivo+ In vitro [189] Anti-cancer effect Osthole 0.05, 0.1, 0.15 mmol/L In vitro [190] Anti-cancer effect Osthole 0, 20, 40, 80, 120, 160, 200 µM In vitro [191] Anti-cancer effect Osthole 0, 20, 80, and 160 µM for 14 days intraperitoneal injection In vivo+ In vitro [192] Table A1. Cont.…”

Section: Pharmacological Effects Tested Substance Active Dose/concentmentioning

confidence: 99%

Phytochemistry, Ethnopharmacology, Pharmacokinetics and Toxicology of Cnidium monnieri (L.) Cusson

Sun

Yang

Lenon

2020

IJMS

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Cnidium monnieri (L.) Cusson (CMC) is a traditional Chinese herbal medicine that has been widely grown and used in Asia. It is also known as “She chuang zi” in China (Chinese: 蛇床子), “Jashoshi” in Japan, “Sasangia” in Korea, and “Xa sang tu” in Vietnam. This study aimed to provide an up-to-date review of its phytochemistry, ethnopharmacology, pharmacokinetics, and toxicology. All available information on CMC was collected from the Encyclopedia of Traditional Chinese Medicines, PubMed, EMBASE, ScienceDirect, Scopus, Web of Science, and China Network Knowledge Infrastructure. The updated chemical structures of the compounds are those ones without chemical ID numbers or references from the previous review. A total of 429 chemical constituents have been elucidated and 56 chemical structures have been firstly identified in CMC with traceable evidence. They can be categorized as coumarins, volatile constituents, liposoluble compounds, chromones, monoterpenoid glucosides, terpenoids, glycosides, glucides, and other compounds. CMC has demonstrated impressive potential for the management of various diseases in extensive preclinical research. Since most of the studies are overly concentrated on osthole, more research is needed to investigate other chemical constituents.

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“…All experiments were repeated at least 3 times and the data were presented as the mean ± standard deviation (SD). The results were analyzed by Student's t-test for the comparison of two and ANOVA (followed by Tukey's post hoc test) for the comparison of multiple samples using SPSS 19.0 software (IBM Corp., Armonk, NY, USA). P<0.05 was considered to indicate a statistically significant result.…”

Section: Real-time Reverse Transcription-quantitative Polymerase Chaimentioning

confidence: 99%

“…PTEN is a tumor suppressor gene that has frequently been reported to be involved in the regulation of cell proliferation, invasion, migration and apoptosis in many types of cancer, and the expression of PTEN is downregulated in a wide range of malignancies, including breast cancer, glioblastoma, colorectal carcinoma, pancreatic cancer and OSCC (13)(14)(15)(16)(17). Previous studies have demonstrated that the PI3K/Akt signaling pathway is involved in multiple biological processes and that PTEN functions as a tumor suppressor by negatively regulating the PI3K/Akt signaling pathway, which reduces cell growth and increases cell apoptosis (18,19). miRNAs, including miR-136, miR-181a and miR-221/222, have been reported to regulate the expression of PTEN (20)(21)(22).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of miR‑21 promotes cell apoptosis in oral squamous cell carcinoma by upregulating PTEN

et al. 2018

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MicroRNA‑21 (miR‑21) has been identified as an oncogene and confirmed to serve an important role in carcinogenesis in various types of cancer. However, the effect and mechanism of miR‑21 in oral squamous cell carcinoma (OSCC) has not been fully elucidated. In the present study, miR‑21 inhibitor and empty vector were transfected into OSCC cells, and non‑transfected cells were used as a blank control. The results indicated that when compared with the control and scramble groups, miR‑21 inhibitor suppressed the expression of miR‑21. Conversely, phosphatase and tensin homolog deletion on chromosome 10 (PTEN) was markedly upregulated, and a dual luciferase reporter assay revealed PTEN to be a target gene of miR‑21. Furthermore, miR‑21 inhibitor decreased the proliferation and invasion and enhanced the apoptosis of OSCC cells. There was no significant difference in cell proliferation, invasion and apoptosis between the control and scramble groups. The present data suggested that there may be a regulatory loop between miR‑21 and PTEN, and that miR‑21 inhibition affected the proliferative, invasive and apoptotic abilities of OSCC cells. These findings indicate that miR‑21 may be a possible novel target in the treatment of OSCC.

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Osthole inhibits the PI3K/AKT signaling pathway via activation of PTEN and induces cell cycle arrest and apoptosis in esophageal squamous cell carcinoma

Cited by 50 publications

References 39 publications

Knockdown of anti-silencing function 1B histone chaperone induces cell apoptosis via repressing PI3K/Akt pathway in prostate cancer

Knockdown of anti-silencing function 1B histone chaperone induces cell apoptosis via repressing PI3K/Akt pathway in prostate cancer

Phytochemistry, Ethnopharmacology, Pharmacokinetics and Toxicology of Cnidium monnieri (L.) Cusson

Inhibition of miR‑21 promotes cell apoptosis in oral squamous cell carcinoma by upregulating PTEN

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