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Triptolide inhibits cell proliferation and tumorigenicity of human neuroblastoma cells.

Yan X, Ke XX, Zhao H, Huang M, Hu R, Cui H - Mol Med Rep (2014)

Bottom Line: Reverse transcription‑quantitative polymerase chain reaction was conducted to detect the expression levels of the apoptosis‑associated proteins, caspase‑3 and caspase‑9.The results demonstrated that exposure of BE(2)‑C human neuroblastoma cells to triptolide resulted in a reduction in cell growth and proliferation, and the induction of cell death and apoptosis, together with cell cycle arrest in the S phase.The xenograft experiment showed that triptolide significantly reduced tumor growth and development in vivo.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400716, P.R. China.

ABSTRACT
Triptolide is a diterpene triepoxide, extracted from the Chinese herb Tripterygium wilfordii Hook F, which has been shown to have antitumor activity in a number of cancers. Neuroblastoma is an aggressive extracranial pediatric solid tumor, with significant chemotherapeutic resistance. In this study, triptolide was hypothesized to be a potential therapeutic agent for neuroblastoma. The effects of triptolide on neuroblastoma cell growth and tumor development were investigated. Cell growth and proliferation were evaluated using a cell counting kit‑8 assay and a 5-bromo-2-deoxyuridine staining assay. Cell cycle and apoptosis were detected by flow cytometry. Reverse transcription‑quantitative polymerase chain reaction was conducted to detect the expression levels of the apoptosis‑associated proteins, caspase‑3 and caspase‑9. The tumorigenicity of neuroblastoma cells was assessed by a soft agar clonogenic assay and an in vivo tumorigenic assay. The results demonstrated that exposure of BE(2)‑C human neuroblastoma cells to triptolide resulted in a reduction in cell growth and proliferation, and the induction of cell death and apoptosis, together with cell cycle arrest in the S phase. A soft agar assay indicated that triptolide inhibited the colony‑forming ability of BE(2)‑C neuroblastoma cells. The xenograft experiment showed that triptolide significantly reduced tumor growth and development in vivo. The data suggested that this Chinese herb may be a potential novel chemotherapeutic agent for neuroblastoma.

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Triptolide inhibited tumor growth and development in the xenograft model. BE(2)-C cells (1×106) were injected subcutaneously into the flanks of NOD/SCID mice. After tumor formation (approximately two weeks), mice were injected with DMSO or triptolide (0.4 mg/kg) daily for seven days. (A) Images of tumors dissected from NOD/SCID mice after treatment with triptolide or DMSO. (B) Xenograft tumors were measured daily, after treatment with triptolide or DMSO, by calipers. (C) Scatter plot of xenograft tumor weight with horizontal lines indicated the mean in each group. (D) The average body weight of NOD/SCID mice was monitored daily after treatment with triptolide or DMSO. Data are presented as the mean ± standard deviation. *P<0.05 and **P<0.01, compared with control. DMSO, dimethyl sulfoxide; NOD mice, non-obese diabetic mice; SCID mice, severe combined immunodeficiency mice.
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f6-mmr-11-02-0791: Triptolide inhibited tumor growth and development in the xenograft model. BE(2)-C cells (1×106) were injected subcutaneously into the flanks of NOD/SCID mice. After tumor formation (approximately two weeks), mice were injected with DMSO or triptolide (0.4 mg/kg) daily for seven days. (A) Images of tumors dissected from NOD/SCID mice after treatment with triptolide or DMSO. (B) Xenograft tumors were measured daily, after treatment with triptolide or DMSO, by calipers. (C) Scatter plot of xenograft tumor weight with horizontal lines indicated the mean in each group. (D) The average body weight of NOD/SCID mice was monitored daily after treatment with triptolide or DMSO. Data are presented as the mean ± standard deviation. *P<0.05 and **P<0.01, compared with control. DMSO, dimethyl sulfoxide; NOD mice, non-obese diabetic mice; SCID mice, severe combined immunodeficiency mice.

Mentions: The role of triptolide in neuroblastoma tumorigenesis was examined. BE(2)-C cells treated with 25 nM triptolide gave rise to smaller and and sparser colonies in soft agar, compared with cells treated with DMSO (Fig. 5A and B). The xenograft study in NOD/SCID mice showed that the volume and weight of xenograft tumors in the triptolide treatment group were lower than those in the DMSO group (Fig. 6). These data indicate that triptolide may inhibit neuroblastoma cell self-renewal and tumorigenesis. In addition, there was no significant difference in mouse body weight after triptolide treatment (Fig. 6D), which suggests that the administered dose of triptolide may have minimal toxic side effects.


Triptolide inhibits cell proliferation and tumorigenicity of human neuroblastoma cells.

Yan X, Ke XX, Zhao H, Huang M, Hu R, Cui H - Mol Med Rep (2014)

Triptolide inhibited tumor growth and development in the xenograft model. BE(2)-C cells (1×106) were injected subcutaneously into the flanks of NOD/SCID mice. After tumor formation (approximately two weeks), mice were injected with DMSO or triptolide (0.4 mg/kg) daily for seven days. (A) Images of tumors dissected from NOD/SCID mice after treatment with triptolide or DMSO. (B) Xenograft tumors were measured daily, after treatment with triptolide or DMSO, by calipers. (C) Scatter plot of xenograft tumor weight with horizontal lines indicated the mean in each group. (D) The average body weight of NOD/SCID mice was monitored daily after treatment with triptolide or DMSO. Data are presented as the mean ± standard deviation. *P<0.05 and **P<0.01, compared with control. DMSO, dimethyl sulfoxide; NOD mice, non-obese diabetic mice; SCID mice, severe combined immunodeficiency mice.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4262511&req=5

f6-mmr-11-02-0791: Triptolide inhibited tumor growth and development in the xenograft model. BE(2)-C cells (1×106) were injected subcutaneously into the flanks of NOD/SCID mice. After tumor formation (approximately two weeks), mice were injected with DMSO or triptolide (0.4 mg/kg) daily for seven days. (A) Images of tumors dissected from NOD/SCID mice after treatment with triptolide or DMSO. (B) Xenograft tumors were measured daily, after treatment with triptolide or DMSO, by calipers. (C) Scatter plot of xenograft tumor weight with horizontal lines indicated the mean in each group. (D) The average body weight of NOD/SCID mice was monitored daily after treatment with triptolide or DMSO. Data are presented as the mean ± standard deviation. *P<0.05 and **P<0.01, compared with control. DMSO, dimethyl sulfoxide; NOD mice, non-obese diabetic mice; SCID mice, severe combined immunodeficiency mice.
Mentions: The role of triptolide in neuroblastoma tumorigenesis was examined. BE(2)-C cells treated with 25 nM triptolide gave rise to smaller and and sparser colonies in soft agar, compared with cells treated with DMSO (Fig. 5A and B). The xenograft study in NOD/SCID mice showed that the volume and weight of xenograft tumors in the triptolide treatment group were lower than those in the DMSO group (Fig. 6). These data indicate that triptolide may inhibit neuroblastoma cell self-renewal and tumorigenesis. In addition, there was no significant difference in mouse body weight after triptolide treatment (Fig. 6D), which suggests that the administered dose of triptolide may have minimal toxic side effects.

Bottom Line: Reverse transcription‑quantitative polymerase chain reaction was conducted to detect the expression levels of the apoptosis‑associated proteins, caspase‑3 and caspase‑9.The results demonstrated that exposure of BE(2)‑C human neuroblastoma cells to triptolide resulted in a reduction in cell growth and proliferation, and the induction of cell death and apoptosis, together with cell cycle arrest in the S phase.The xenograft experiment showed that triptolide significantly reduced tumor growth and development in vivo.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400716, P.R. China.

ABSTRACT
Triptolide is a diterpene triepoxide, extracted from the Chinese herb Tripterygium wilfordii Hook F, which has been shown to have antitumor activity in a number of cancers. Neuroblastoma is an aggressive extracranial pediatric solid tumor, with significant chemotherapeutic resistance. In this study, triptolide was hypothesized to be a potential therapeutic agent for neuroblastoma. The effects of triptolide on neuroblastoma cell growth and tumor development were investigated. Cell growth and proliferation were evaluated using a cell counting kit‑8 assay and a 5-bromo-2-deoxyuridine staining assay. Cell cycle and apoptosis were detected by flow cytometry. Reverse transcription‑quantitative polymerase chain reaction was conducted to detect the expression levels of the apoptosis‑associated proteins, caspase‑3 and caspase‑9. The tumorigenicity of neuroblastoma cells was assessed by a soft agar clonogenic assay and an in vivo tumorigenic assay. The results demonstrated that exposure of BE(2)‑C human neuroblastoma cells to triptolide resulted in a reduction in cell growth and proliferation, and the induction of cell death and apoptosis, together with cell cycle arrest in the S phase. A soft agar assay indicated that triptolide inhibited the colony‑forming ability of BE(2)‑C neuroblastoma cells. The xenograft experiment showed that triptolide significantly reduced tumor growth and development in vivo. The data suggested that this Chinese herb may be a potential novel chemotherapeutic agent for neuroblastoma.

Show MeSH
Related in: MedlinePlus