Norcantharidin

CAS# 5442-12-6

Norcantharidin

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Quality Control of Norcantharidin

Number of papers citing our products

Chemical structure

Norcantharidin

3D structure

Chemical Properties of Norcantharidin

Cas No. 5442-12-6 SDF Download SDF
PubChem ID 93004 Appearance White powder
Formula C8H8O4 M.Wt 168.15
Type of Compound Monoterpenoids Storage Desiccate at -20°C
Synonyms Norcantharadine; 29745-04-8
Solubility Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
SMILES C1CC2C3C(C1O2)C(=O)OC3=O
Standard InChIKey JAABVEXCGCXWRR-UHFFFAOYSA-N
Standard InChI InChI=1S/C8H8O4/c9-7-5-3-1-2-4(11-3)6(5)8(10)12-7/h3-6H,1-2H2
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Norcantharidin

The polypides of Mylabris phalerata Pallas

Biological Activity of Norcantharidin

DescriptionNorcantharidin has been used to treat human cancers in China since 1984, it inhibits the canonical Wnt signal pathway in NSCLC, by activating WIF-1 via promoter demethylation; it also enhances TIMP‑2 antitumor and anti‑vasculogenic mimicry activities in GBCs through downregulating MMP‑2 and MT1‑MMP. Norcantharidin is a protein phosphatase type-2A inhibitor, which has less nephrotoxic and phlogogenic side-effects, it can inhibit both DNA synthesis and granulocyte-macrophage colony-forming cells (GM-CFC)growth and impaire the neogenesis of chromatin material and nuclear membrane during the M/G1 phase transition in K-562 cells.
TargetsMMP(e.g.TIMP) | VEGFR | PKC | Wnt/β-catenin | Caspase | Bcl-2/Bax | DNA/RNA Synthesis | p53
In vitro

Norcantharidin inhibits lymphangiogenesis by downregulating the expression of VEGF-C and VEGF-D in human dermal lymphatic endothelial cells in vitro.[Pubmed: 25572616]

Pharmacology. 2015;95(1-2):1-9.

To investigate the effects of Norcantharidin on the growth and migration of human dermal lymphatic endothelial cells (HDLECs) and further characterize its effect on lymphangiogenesis.
METHODS AND RESULTS:
A 3-dimensional fibrin gel lymphangiogenesis model was built. Flow cytometry was used to analyze the rate of apoptosis and necrosis. RT-PCR, immunohistochemistry and immunoblotting assays were used to examine the effect of Norcantharidin on vascular endothelial growth factor C (VEGF-C), VEGF-D and VEGF receptor 3 during in vitro lymphangiogenesis. Norcantharidin caused a marked dose and time-dependent inhibition of the growth of HDLECs with an IC50 of 40 nmol/l. The apoptotic rate of HDLECs was 13.21 ± 1.60% 24 h after treatment with 7.5 nmol/l Norcantharidin and 42.34 ± 3.80% with 90 nmol/l Norcantharidin (p < 0.01 vs. controls in both). Fibrin gel assays showed that Norcantharidin (15 nmol/l) reduced the number of tubular structures from 68.4 ± 5.2 in untreated controls to 10.9 ± 2.3 (p = 0.000). RT-PCR, immunohistochemistry and immunoblotting assays showed Norcantharidin markedly reduced the expression of VEGF-C and VEGF-D.
CONCLUSIONS:
Norcantharidin inhibits lymphangiogenesis by downregulating the expression of VEGF-C and VEGF-D, suggesting that Norcantharidin could be an effective agent for targeting neolymphangiogenesis.

Norcantharidin-induced apoptosis in oral cancer cells is associated with an increase of proapoptotic to antiapoptotic protein ratio.[Pubmed: 15596295 ]

Cancer Lett. 2005 Jan 10;217(1):43-52.

Norcantharidin (NCTD), the demethylated analogue of cantharidin, has been used to treat human cancers in China since 1984. It was recently found to be capable of inducing apoptosis in human colon carcinoma, hepatoma and glioblastoma cells by way of an elusive mechanism.
METHODS AND RESULTS:
In this study, we demonstrated that NCTD also induces apoptosis in human oral cancer cell lines SAS (p53 wild-type phenotype) and Ca9-22 (p53 mutant) as evidenced by nuclear condensation, TUNEL labeling, DNA fragmentation and cleavage of PARP. Apoptosis induced by NCTD was both dose- and time-dependent. We found NCTD did not induce Fas and FasL, implying that it activated other apoptosis pathways. Our data showed that NCTD caused accumulation of cytosolic cytochrome c and activation of caspase-9, suggesting that apoptosis occurred via the mitochondria mediated pathway. NCTD enhanced the expression of Bax in SAS cells consistent with their p53 status. Moreover, we showed that NCTD downregulated the expression of Bcl-2 in Ca9-22 and Bcl-XL in SAS.
CONCLUSIONS:
Our results suggest that NCTD-induced apoptosis in oral cancer cells may be mediated by an increase in the ratios of proapoptotic to antiapoptotic proteins. Since oral cancer cells with mutant p53 or elevated Bcl-XL levels showed resistance to multiple chemotherapeutic agents, NCTD may overcome the chemoresistance of these cells and provide potential new avenues for treatment.

In vivo

Norcantharidin enhances TIMP‑2 anti‑vasculogenic mimicry activity for human gallbladder cancers through downregulating MMP‑2 and MT1‑MMP.[Pubmed: 25405519]

Int J Oncol. 2015 Feb;46(2):627-40.

Vasculogenic mimicry (VM) is a tumor microcirculation pattern in highly aggressive gallbladder cancers (GBCs). We recently reported the anti‑VM activity of Norcantharidin (NCTD) in highly aggressive GBC‑SD cells and xenografts.
METHODS AND RESULTS:
In this study, we further investigated that Norcantharidin enhanced tissue inhibitor of matrix metalloproteinase‑2 (TIMP‑2) anti‑VM activity for GBCs and the underlying mechanisms. In vivo and in vitro experiments were performed to determine the effects of Norcantharidin in combination with TIMP‑2 on tumor growth, host survival, VM formation, hemodynamic of GBC‑SD xenografts, and VM‑like networks and malignant phenotypes of GBC‑SD cells. Expression of matrix metalloproteinase (MMP)‑2 and membrane type 1‑MMP (MT1‑MMP) among human GBCs, GBC‑SD cells and xenografts were determined, respectively. The results showed that expression of MMP‑2 and MT1‑MMP in human GBCs, GBC‑SD cells and xenografts was significantly related to VM in GBCs; a shorter survival time of VM‑positive patients with high expression of MMP‑2 or MT1‑MMP compared to that of the patients with low expression. After treatment with Norcantharidin +TIMP‑2, tumor growth, VM formation, VM hemodynamic of the xenografts in vivo were significantly inhibited as compared to control, Norcantharidin or TIMP‑2 group, with a prolonged survival time of the xenograft mice (log‑rank test, P=0.0115); and these observations were confirmed by VM‑like networks by 3‑D matrices and showed that proliferation, apoptosis, invasion, migration of GBC‑SD cells in vitro were markedly affected. Furthermore, expression of MMP‑2 and MT1‑MMP in VM formation of the xenografts in vivo and GBC‑SD cells in vitro was downregulated as compared to control, Norcantharidin or TIMP‑2 group.
CONCLUSIONS:
Thus, we concluded that Norcantharidin enhances TIMP‑2 antitumor and anti‑VM activities in GBCs through downregulating MMP‑2 and MT1‑MMP.

Effects of norcantharidin, a protein phosphatase type-2A inhibitor, on the growth of normal and malignant haemopoietic cells.[Pubmed: 7646929]

Eur J Cancer. 1995 Jun;31A(6):953-63.

Cantharidin is a natural toxin that inhibits protein phosphatase type 2A (PP2A) and has antitumour effects in man. We have studied the synthetic analogue, Norcantharidin (NCTD), which has less nephrotoxic and phlogogenic side-effects, investigating the effects on the normal haemopoietic system and leukaemia cell growth.
METHODS AND RESULTS:
Daily intraperitoneal (i.p.) injection of NCTD induced dose and circadian time-dependent transient leucocytosis in normal mice, but did not accelerate bone marrow (BM) regeneration, or have haemopoietic offe-effects following chronic administration. NCTD stimulated the cell cycle progression of granulocyte-macrophage colony-forming cells (GM-CFC), stimulated DNA synthesis and increased the frequency of mitotic cells in short-term human BM cultures. NCTD also stimulated the production of interleukin (IL)-1 beta, colony stimulating activity (CSA) and tumour necrosis factor (TNF)-alpha. Continuous in vitro NCTD treatment, however, inhibited both DNA synthesis and GM-CFC growth. Fluorescence-activated cell sorting (FACS) analysis of DNA profiles and cytological studies in HL-60, K-562 or MRC5V2 (fibroblast) cells indicated that low doses of NCTD accelerated the G1/S phase transition, while higher doses or prolonged incubations inhibited the cell cycle at the G2/M phases or during the formation of postmitotic daughter cells. Electron microscopy revealed that NCTD impaired the neogenesis of chromatin material and nuclear membrane during the M/G1 phase transition in K-562 cells. The biphasic effect of NCTD may be due to inhibition of PP2A activity, which regulates the cell cycle, both at the restriction point and at the G2 and M phases.
CONCLUSIONS:
Our data provide new insight into the cellular and molecular actions of NCTD, and partly explain its therapeutical effects in cancer patients.

Protocol of Norcantharidin

Kinase Assay

Norcantharidin inhibits Wnt signal pathway via promoter demethylation of WIF-1 in human non-small cell lung cancer.[Pubmed: 25814287]

Tamoxifen enhances the anticancer effect of cantharidin and norcantharidin in pancreatic cancer cell lines through inhibition of the protein kinase C signaling pathway.[Pubmed: 25624908]

Oncol Lett. 2015 Feb;9(2):837-844. Epub 2014 Nov 19.

Cantharidin is an active constituent of mylabris, a traditional Chinese therapeutic agent. Cantharidin is a potent and selective inhibitor of protein phosphatase 2A (PP2A). Cantharidin has been previously reported to efficiently repress the growth of pancreatic cancer cells. However, excessively activated protein kinase C (PKC) has been shown to improve cell survival following the adminstration of cantharidin. Tamoxifen is widely used in the treatment of estrogen receptor-positive breast cancer. In addition, an increasing number of studies have found that tamoxifen selectively inhibits PKC and represses growth in estrogen receptor-negative cancer cells. Administration of a combination of PKC inhibitor and PP2A inhibitors has been demonstrated to exert a synergistic anticancer effect.
METHODS AND RESULTS:
The proliferation of pancreatic cancer cells was analyzed by 3-(4,5-dimethyltiazol-2-yl]2, 5-diphenyltetrazo-lium bromide assay. The expression levels of ERα and ERβ in various pancreatic cancer cell lines were determined by reverse transcription polymerase chain reaction. In addition, the protein levels of PKCα and phosphorylated PKCα in pancreatic cell lines were analyzed by western blot analysis. In the present study, tamoxifen was found to exert a cytotoxic effect against pancreatic cancer cells independent of the hormone receptor status. Tamoxifen repressed the phosphorylation of PKC, and amplified the anticancer effect induced by cantharidin and Norcantharidin.
CONCLUSIONS:
The findings reveal a novel potential strategy against pancreatic cancer using co-treatment with tamoxifen plus cantharidin or cantharidin derivatives.

Med Oncol. 2015 May;32(5):592.

Wingless-type (Wnt) family of secreted glycoproteins is a group of signal molecules implicated in oncogenesis. Abnormal activation of Wnt signal pathway is associated with a variety of human cancers, including non-small cell lung cancer (NSCLC). Wnt antagonists, such as the secreted frizzled-related protein (SFRP) family, Wnt inhibitory factor-1 (WIF-1) and cerberus, inhibit Wnt signal pathway by directly binding to Wnt molecules. Norcantharidin (NCTD) is known to possess anticancer activity but less nephrotoxicity than cantharidin.
METHODS AND RESULTS:
In this study, we found that NCTD inhibited cell proliferation, induced apoptosis, arrested cell cycle and suppressed cell invasion/migration in vitro. Additionally, Wnt signal pathway transcription was also suppressed. NCTD treatment blocked cytoplasmic translocation of beta-catenin into the nucleus. Alterations of apoptosis-related proteins, such as Bax, cleaved caspase-3 (pro-apoptotic) and Bcl-2 (anti-apoptotic), had been detected. Furthermore, the expression levels of WIF-1 and SFRP1 were significantly increased in NCTD-treated groups compared with negative control (NC) groups. Abnormal methylation was observed in NC groups, while NCTD treatment promoted WIF-1 demethylation.
CONCLUSIONS:
The present study revealed that NCTD activated WIF-1 via promoter demethylation, inhibiting the canonical Wnt signal pathway in NSCLC, which may present a new therapeutic target in vivo.

Norcantharidin Dilution Calculator

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Preparing Stock Solutions of Norcantharidin

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 5.9471 mL 29.7354 mL 59.4707 mL 118.9414 mL 148.6768 mL
5 mM 1.1894 mL 5.9471 mL 11.8941 mL 23.7883 mL 29.7354 mL
10 mM 0.5947 mL 2.9735 mL 5.9471 mL 11.8941 mL 14.8677 mL
50 mM 0.1189 mL 0.5947 mL 1.1894 mL 2.3788 mL 2.9735 mL
100 mM 0.0595 mL 0.2974 mL 0.5947 mL 1.1894 mL 1.4868 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on Norcantharidin

Norcantharidin enhances TIMP2 antivasculogenic mimicry activity for human gallbladder cancers through downregulating MMP2 and MT1MMP.[Pubmed:25405519]

Int J Oncol. 2015 Feb;46(2):627-40.

Vasculogenic mimicry (VM) is a tumor microcirculation pattern in highly aggressive gallbladder cancers (GBCs). We recently reported the antiVM activity of Norcantharidin (NCTD) in highly aggressive GBCSD cells and xenografts. In this study, we further investigated that NCTD enhanced tissue inhibitor of matrix metalloproteinase2 (TIMP2) antiVM activity for GBCs and the underlying mechanisms. In vivo and in vitro experiments were performed to determine the effects of NCTD in combination with TIMP2 on tumor growth, host survival, VM formation, hemodynamic of GBCSD xenografts, and VMlike networks and malignant phenotypes of GBCSD cells. Expression of matrix metalloproteinase (MMP)2 and membrane type 1MMP (MT1MMP) among human GBCs, GBCSD cells and xenografts were determined, respectively. The results showed that expression of MMP2 and MT1MMP in human GBCs, GBCSD cells and xenografts was significantly related to VM in GBCs; a shorter survival time of VMpositive patients with high expression of MMP2 or MT1MMP compared to that of the patients with low expression. After treatment with NCTD+TIMP2, tumor growth, VM formation, VM hemodynamic of the xenografts in vivo were significantly inhibited as compared to control, NCTD or TIMP2 group, with a prolonged survival time of the xenograft mice (logrank test, P=0.0115); and these observations were confirmed by VMlike networks by 3D matrices and showed that proliferation, apoptosis, invasion, migration of GBCSD cells in vitro were markedly affected. Furthermore, expression of MMP2 and MT1MMP in VM formation of the xenografts in vivo and GBCSD cells in vitro was downregulated as compared to control, NCTD or TIMP2 group. Thus, we concluded that NCTD enhances TIMP2 antitumor and antiVM activities in GBCs through downregulating MMP2 and MT1MMP.

Norcantharidin-induced apoptosis in oral cancer cells is associated with an increase of proapoptotic to antiapoptotic protein ratio.[Pubmed:15596295]

Cancer Lett. 2005 Jan 10;217(1):43-52.

Norcantharidin (NCTD), the demethylated analogue of cantharidin, has been used to treat human cancers in China since 1984. It was recently found to be capable of inducing apoptosis in human colon carcinoma, hepatoma and glioblastoma cells by way of an elusive mechanism. In this study, we demonstrated that NCTD also induces apoptosis in human oral cancer cell lines SAS (p53 wild-type phenotype) and Ca9-22 (p53 mutant) as evidenced by nuclear condensation, TUNEL labeling, DNA fragmentation and cleavage of PARP. Apoptosis induced by NCTD was both dose- and time-dependent. We found NCTD did not induce Fas and FasL, implying that it activated other apoptosis pathways. Our data showed that NCTD caused accumulation of cytosolic cytochrome c and activation of caspase-9, suggesting that apoptosis occurred via the mitochondria mediated pathway. NCTD enhanced the expression of Bax in SAS cells consistent with their p53 status. Moreover, we showed that NCTD downregulated the expression of Bcl-2 in Ca9-22 and Bcl-XL in SAS. Our results suggest that NCTD-induced apoptosis in oral cancer cells may be mediated by an increase in the ratios of proapoptotic to antiapoptotic proteins. Since oral cancer cells with mutant p53 or elevated Bcl-XL levels showed resistance to multiple chemotherapeutic agents, NCTD may overcome the chemoresistance of these cells and provide potential new avenues for treatment.

Tamoxifen enhances the anticancer effect of cantharidin and norcantharidin in pancreatic cancer cell lines through inhibition of the protein kinase C signaling pathway.[Pubmed:25624908]

Oncol Lett. 2015 Feb;9(2):837-844.

Cantharidin is an active constituent of mylabris, a traditional Chinese therapeutic agent. Cantharidin is a potent and selective inhibitor of protein phosphatase 2A (PP2A). Cantharidin has been previously reported to efficiently repress the growth of pancreatic cancer cells. However, excessively activated protein kinase C (PKC) has been shown to improve cell survival following the adminstration of cantharidin. Tamoxifen is widely used in the treatment of estrogen receptor-positive breast cancer. In addition, an increasing number of studies have found that tamoxifen selectively inhibits PKC and represses growth in estrogen receptor-negative cancer cells. Administration of a combination of PKC inhibitor and PP2A inhibitors has been demonstrated to exert a synergistic anticancer effect. The proliferation of pancreatic cancer cells was analyzed by 3-(4,5-dimethyltiazol-2-yl]2, 5-diphenyltetrazo-lium bromide assay. The expression levels of ERalpha and ERbeta in various pancreatic cancer cell lines were determined by reverse transcription polymerase chain reaction. In addition, the protein levels of PKCalpha and phosphorylated PKCalpha in pancreatic cell lines were analyzed by western blot analysis. In the present study, tamoxifen was found to exert a cytotoxic effect against pancreatic cancer cells independent of the hormone receptor status. Tamoxifen repressed the phosphorylation of PKC, and amplified the anticancer effect induced by cantharidin and Norcantharidin. The findings reveal a novel potential strategy against pancreatic cancer using co-treatment with tamoxifen plus cantharidin or cantharidin derivatives.

Norcantharidin inhibits Wnt signal pathway via promoter demethylation of WIF-1 in human non-small cell lung cancer.[Pubmed:25814287]

Med Oncol. 2015 May;32(5):145.

Wingless-type (Wnt) family of secreted glycoproteins is a group of signal molecules implicated in oncogenesis. Abnormal activation of Wnt signal pathway is associated with a variety of human cancers, including non-small cell lung cancer (NSCLC). Wnt antagonists, such as the secreted frizzled-related protein (SFRP) family, Wnt inhibitory factor-1 (WIF-1) and cerberus, inhibit Wnt signal pathway by directly binding to Wnt molecules. Norcantharidin (NCTD) is known to possess anticancer activity but less nephrotoxicity than cantharidin. In this study, we found that NCTD inhibited cell proliferation, induced apoptosis, arrested cell cycle and suppressed cell invasion/migration in vitro. Additionally, Wnt signal pathway transcription was also suppressed. NCTD treatment blocked cytoplasmic translocation of beta-catenin into the nucleus. Alterations of apoptosis-related proteins, such as Bax, cleaved caspase-3 (pro-apoptotic) and Bcl-2 (anti-apoptotic), had been detected. Furthermore, the expression levels of WIF-1 and SFRP1 were significantly increased in NCTD-treated groups compared with negative control (NC) groups. Abnormal methylation was observed in NC groups, while NCTD treatment promoted WIF-1 demethylation. The present study revealed that NCTD activated WIF-1 via promoter demethylation, inhibiting the canonical Wnt signal pathway in NSCLC, which may present a new therapeutic target in vivo.

Norcantharidin inhibits lymphangiogenesis by downregulating the expression of VEGF-C and VEGF-D in human dermal lymphatic endothelial cells in vitro.[Pubmed:25572616]

Pharmacology. 2015;95(1-2):1-9.

AIMS: To investigate the effects of Norcantharidin on the growth and migration of human dermal lymphatic endothelial cells (HDLECs) and further characterize its effect on lymphangiogenesis. METHODS: A 3-dimensional fibrin gel lymphangiogenesis model was built. Flow cytometry was used to analyze the rate of apoptosis and necrosis. RT-PCR, immunohistochemistry and immunoblotting assays were used to examine the effect of Norcantharidin on vascular endothelial growth factor C (VEGF-C), VEGF-D and VEGF receptor 3 during in vitro lymphangiogenesis. RESULTS: Norcantharidin caused a marked dose and time-dependent inhibition of the growth of HDLECs with an IC50 of 40 nmol/l. The apoptotic rate of HDLECs was 13.21 +/- 1.60% 24 h after treatment with 7.5 nmol/l Norcantharidin and 42.34 +/- 3.80% with 90 nmol/l Norcantharidin (p < 0.01 vs. controls in both). Fibrin gel assays showed that Norcantharidin (15 nmol/l) reduced the number of tubular structures from 68.4 +/- 5.2 in untreated controls to 10.9 +/- 2.3 (p = 0.000). RT-PCR, immunohistochemistry and immunoblotting assays showed Norcantharidin markedly reduced the expression of VEGF-C and VEGF-D. CONCLUSION: Norcantharidin inhibits lymphangiogenesis by downregulating the expression of VEGF-C and VEGF-D, suggesting that Norcantharidin could be an effective agent for targeting neolymphangiogenesis.

Effects of norcantharidin, a protein phosphatase type-2A inhibitor, on the growth of normal and malignant haemopoietic cells.[Pubmed:7646929]

Eur J Cancer. 1995 Jun;31A(6):953-63.

Cantharidin is a natural toxin that inhibits protein phosphatase type 2A (PP2A) and has antitumour effects in man. We have studied the synthetic analogue, Norcantharidin (NCTD), which has less nephrotoxic and phlogogenic side-effects, investigating the effects on the normal haemopoietic system and leukaemia cell growth. Daily intraperitoneal (i.p.) injection of NCTD induced dose and circadian time-dependent transient leucocytosis in normal mice, but did not accelerate bone marrow (BM) regeneration, or have haemopoietic offe-effects following chronic administration. NCTD stimulated the cell cycle progression of granulocyte-macrophage colony-forming cells (GM-CFC), stimulated DNA synthesis and increased the frequency of mitotic cells in short-term human BM cultures. NCTD also stimulated the production of interleukin (IL)-1 beta, colony stimulating activity (CSA) and tumour necrosis factor (TNF)-alpha. Continuous in vitro NCTD treatment, however, inhibited both DNA synthesis and GM-CFC growth. Fluorescence-activated cell sorting (FACS) analysis of DNA profiles and cytological studies in HL-60, K-562 or MRC5V2 (fibroblast) cells indicated that low doses of NCTD accelerated the G1/S phase transition, while higher doses or prolonged incubations inhibited the cell cycle at the G2/M phases or during the formation of postmitotic daughter cells. Electron microscopy revealed that NCTD impaired the neogenesis of chromatin material and nuclear membrane during the M/G1 phase transition in K-562 cells. The biphasic effect of NCTD may be due to inhibition of PP2A activity, which regulates the cell cycle, both at the restriction point and at the G2 and M phases. Our data provide new insight into the cellular and molecular actions of NCTD, and partly explain its therapeutical effects in cancer patients.

Description

Norcantharidin is an endogenous metabolite.

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