Enhanced Anti-tumor Efficacy of Aspirin Combined with Triptolide in Cervical Cancer Cells

Chen, Rong-Hui; Yongjie, Tian

doi:10.7314/apjcp.2013.14.5.3041

Cited by 8 publications

(6 citation statements)

References 29 publications

(38 reference statements)

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“…The mechanism of anti-proliferation is related to cell cycle arrest in the S phase, which affects the expression of cyclin B1 and changes the phosphorylation of P34 (49,50).…”

Section: Discussionmentioning

confidence: 99%

Bufalin suppresses esophageal squamous cell carcinoma progression by activating the PIAS3/STAT3 signaling pathway

Ju¹,

Shi²,

Liu³

et al. 2023

J Thorac Dis

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Background: Esophageal cancer, especially esophageal squamous cell carcinoma (ESCC), is a common malignant tumor of the digestive tract. Bufalin is an effective anti-tumor compound. However, little is known about the regulatory mechanisms of Bufalin in ESCC. To investigate the effect and molecular mechanism of Bufalin on the proliferation, migration and invasion of ESCC cells will provide a more reliable basis for the application of Bufalin in clinical tumor therapy.Methods: First, the half-inhibitory concentration (IC50) of Bufalin was evaluated by Cell Counting Kit-8 (CCK-8) assays. In vitro, the effects of Bufalin on the proliferation of the ECA109 cells was measured using CCK-8 and 5-ethynyl-2'-deoxyuridine assays. Wound-healing and transwell assays were used to evaluate the effects of Bufalin on the migration and invasion of the ECA109 cells. Further, to determine the mechanisms underlying the Bufalin-mediated suppression of cell progression in ESCC, total RNA was extracted from negative control (NC) and Bufalin treated cells to perform RNA-sequencing (RNA-seq) to screen for abnormally expressed genes. In vivo, the ECA 109 cells were subcutaneously injected into BALB/c nude mice to determine the effects of Bufalin on tumor cell proliferation. The protein inhibitor of activated signal transducer and activator of transcription 3 (PIAS3), signal transducer and activator of transcription 3 (STAT3), and phosphorylated STAT3 (p-STAT3) protein expression levels in the ECA109 cells were detected by Western blot. Results:The CCK-8 assays showed that the IC50 of Bufalin was 200 nM. The proliferation, migration, and invasion ability of the ECA109 cells was significantly inhibited in the Bufalin group in a concentrationdependent manner. In vivo, the Xenograft tumor model showed that Bufalin decreased the tumor volume and weight of the subcutaneous tumors. The RNA-seq results showed that the expression of PIAS3 was upregulated in the Bufalin group. Additionally, down-regulation of PIAS3 decreased the inhibition of STAT3, thereby increasing p-STAT3 expression. Finally, PIAS3 knockdown reversed the inhibitory effects of Bufalin on the proliferation, migration, and invasion of the ECA109 cells.Conclusions: Bufalin may inhibit the proliferation, migration, and invasion of the ECA109 cells through the PIAS3/STAT3 signaling pathway.

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“…The mechanism of anti-proliferation is related to cell cycle arrest in the S phase, which affects the expression of cyclin B1 and changes the phosphorylation of P34 (49,50).…”

Section: Discussionmentioning

confidence: 99%

Bufalin suppresses esophageal squamous cell carcinoma progression by activating the PIAS3/STAT3 signaling pathway

Ju¹,

Shi²,

Liu³

et al. 2023

J Thorac Dis

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show abstract

“…Apart from its own biological activities triptolide modulates the activity of different popular commercial antitumor drugs that indicates its chemo-sensitizing property. [54][55][56][57][58][59] A major problem associated with the anti-tumor activity of triptolide is its lower solubility in water and greater cytotoxicity that limits its use of clinical study. Therefore, to increase its bioavailability, Xu and colleagues 88 developed polymeric micelles that reduce the triptolide toxicity and increase Poly (D, L-lactic acid) nanoparticles are another very promising carripaire for triptolide that can reduce renal toxicity in rats.…”

Section: Resultsmentioning

confidence: 99%

“…Co-treatment significantly decreased the expression of Bcl 2 and cyclin E gene and increased Bax and p21 gene expression at mRNA level. 55 Lin and co-workers 56 demonstrated that triptolide enhanced the anti-tumor potential of anti-angiogenic drug vasostatin120-180 (VAS). Combined therapy enhances the apoptosis efficacy of VAS by down regulating NF-kB and many anti-apoptotic genes (e.g.…”

Section: Combination Therapymentioning

confidence: 99%

Triptolide Mediated Amelioration of Breast Cancer via Modulation of Molecular Pathways

Sarkar

Paul

2017

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Triptolide is the main bioactive molecule isolated from a root extract of Tripterigium wilfordii Hook F. of Celastraceae family. Chemically, it is a diterpenoid triepoxide molecule and its chemical formula is C 20 H 24 O 6 . Its five-membered unsaturated lactone ring (D-ring) is crucial for anti-tumor potential and carbonyl group at C-18 position is essential to exert important influence on the interaction between triptolide and the targeted protein(s). It is bio-synthesized from deoxy-D-xylullose-5-phosphate (DOXP) pathway in the cell. Triptolide can induce apoptosis in a number of breast cancer cells by up-regulating different pro-apoptotic and down-regulating different anti-apoptotic molecules. In vitro experiments indicate that it can down regulate several cell cycle related genes and induces S-phase cell cycle arrest. Triptolide treatment can also modulate the expression of different cell signaling molecules, e.g. ERK, NF-κB, FAK, VEGF, β-catenin, AKT etc. In vivo experiments indicate that triptolide can effectively reduce breast tumor growth in the mouse model. Apart from the single drug treatment, triptolide can effectively be applied in combination therapy. Application of Triptolide with other chemotherapeutic drugs, very efficiently check the proliferation of tumor cells which reduces the effective concentration of the commercially available drugs thus reducing their toxic sideeffects. Although triptolide is very effective against a number of diseases, its higher degree of multi-organ toxicity limits its use of further clinical trial. Therefore, to reduce the toxic effects, a number of strategies have been developed which increase its water solubility and at the same time decrease the toxic effect. In this review article, we have addressed how triptolide participates in the antitumor processes in breast can cer cells.

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“…Previous studies have shown that NSAIDs play significant role in apoptosis and caspase enzymes activation in cancer cells including cervical cancer cells [5], [6]. The aim of this study was to evaluate the effects of IC50 dose of aspirin on caspase 9 activity level in cervical cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Caspase 9 Activity Level in Hela Cell Line Exposed to Cytotoxic Dose of Aspirin

2018

AEBMS-2017, ICCET-2017, BBMPS-17, UPACEE-17, LHESS-17, TBFIS-2017, IC4E-2017, AMLIS-2017 &Amp; BEFM-2017

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Enhanced Anti-tumor Efficacy of Aspirin Combined with Triptolide in Cervical Cancer Cells

Cited by 8 publications

References 29 publications

Bufalin suppresses esophageal squamous cell carcinoma progression by activating the PIAS3/STAT3 signaling pathway

Bufalin suppresses esophageal squamous cell carcinoma progression by activating the PIAS3/STAT3 signaling pathway

Triptolide Mediated Amelioration of Breast Cancer via Modulation of Molecular Pathways

Evaluation of Caspase 9 Activity Level in Hela Cell Line Exposed to Cytotoxic Dose of Aspirin

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