• 약학회지
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• 제43권5호
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• pp.629-634
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• 1999

A protein-polysaccharide fraction was isolated from the mycelial culture of a Korean basidiomycetous fungus, Hebeloma crustuliniforme, and was named HCA (Hebeloma crustulineforme fraction A). When intraperitoneally injected at 200 mg/kg/day once daily for 10 days, HCA inhibited the growth of sarcoma 180 solid tumor in ICR mice by 65.1% (p＜0.05). HCA also exerted protective effect against leukopenia induced by cyclophosphamide with the protection ratio of 39.7% (p＜0.01).

• KSBB Journal
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• 제17권6호
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• pp.520-524
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• 2002

초석잠의 항암효과 및 면역조절자로서의 기능을 알아보기 위하여 마우스를 이동하여 실험한 결과, 마우스 비장세포의 증식반응은 항진시켰으나 YAC-1 세포주의 증식능은 억제시켰다. CD4+ T세포 및 CD8+ T세포의 비율이 정상 대조군 마우스의 그것에 비하여 증가하였으나 CD4+/CD8+ 비는 차이가 없었으며 비장세포에서 IL-2수용체의 발현이 항진되었다. 또한, 복강대식세포로부터의 nitric oxide와 TNF-$\alpha$ 생산을 항진시켰으며, 복강대식세포는 탐식능이 현저하게 항진되었고 B16F10 흑색종의 폐전이가 억제됨을 알 수 있었다. 따라서, 초석잠의 항암제 및 면역반응 조절자로서의 개발 가능성이 있음을 시사한다.

• 약학회지
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• 제42권4호
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• pp.388-394
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• 1998

The lectin from starfish, Asterina pectinifera, was purified and tested for its potential antitumor activity. It was shown to possess considerable toxicity toward various tumor cell lines. Concentration of Asterina pectinifera lectin (APL) at 4mg/$5{\times}10^5$ cells resulted in 28% death of Ehrlich ascites tumor cell, 40% of L929, 60% of A549, and 52% of HeLa cells after 48 hours incubation. Toxicity of APL to L929, Ehrlich ascites, A549, and HeLa cells revealed a reduction in cell viability of approximately 70% at APL concentration of 8mg/$5{\times}10^5$ cells after 48 hours incubation. Administration of APL ($100{\mu}g/day$ or $300{\mu}g/day$) inhibited the growth of Ehrlich ascites cells in vivo. Mice given only Ehrlich cells survived an average of $15{\pm}1$ (S.E.) days. Mice given Ehrlich cells and $100{\mu}g\;or\;300{\mu}g$ APL had 58% and 67% survival, respectively, after 20 days. These results suggest that APL has antitumor activity.

• 약학회지
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• 제44권4호
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• pp.347-353
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• 2000

To examine influence of artificial digestive juice on the antitumor activity of Ganoderma lucidum-A(GL-A), protein-bound polysaccharide from Ganoderma lucidum, we compared the digested protein-bound polysaccharide with undigested one both on immunopotentiating activity and influence of digestive juices. Protein-bound polysaccharide GL-B was obtained by digesting the antitumor component GL-A with artificial digestive Juices in vitro. When GL-A was administered orally to sarcoma 180 tumor-bearing ICR mice, the life prolonging effect was exhibited in a dose dependent manner Not only GL-A but GL-B increased the production of colony forming unit (CFU) to 10- and 8-fold of that of the control, respectively. Both of the protein-bound polysaccharides also showed the secretion of nitric oxide in RAW 264.7 cell lines to 3.5-and 3.7-fold of that of the control, respectively: GL-A activated components of the alternative complement pathway, whereas GL-B did not. In humoral immunity GL-A increased the activity of alkaline phosphatase in differentiated B cells to 3 times and GL-B to 4 times of that of the control. These results showed that the artificial digestive juices had no influence on the antitumor activity of the protein-bound polysaccharide from Ganoderma lucidum and that its immunomodulating activity retained after treatment with artificial digestive juice. And this provides a basis of the protein-bound polysaccharide of Ganoderma lucidum as an peroral anticancer drug.

• Biomolecules & Therapeutics
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• 제27권5호
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• pp.484-491
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• 2019

Glioblastoma is the most aggressive common brain tumor in adults. Curcumin, from Curcuma longa, is an effective antitumor agent. Although the same proteins control both autophagy and cell death, the molecular connections between them are complicated and autophagy may promote or inhibit cell death. We investigated whether curcumin affects autophagy, which regulates curcumin-mediated tumor cell death in A172 human glioblastoma cells. When A172 cells were incubated with $10{\mu}M$ curcumin, autophagy increased in a time-dependent manner. Curcumin-induced cell death was reduced by co-incubation with the autophagy inhibitors 3-methyladenine (3-MA), hydroxychloroquine (HCQ), and LY294002. Curcumin-induced cell death was also inhibited by co-incubation with rapamycin, an autophagy inducer. When cells were incubated under serum-deprived medium, LC3-II amount was increased but the basal level of cell viability was reduced, leading to the inhibition of curcumin-induced cell death. Cell death was decreased by inhibiting curcumin-induced autophagy using small interference RNA (siRNA) of Atg5 or Beclin1. Therefore, curcumin-mediated tumor cell death is promoted by curcumin-induced autophagy, but not by an increase in the basal level of autophagy in rapamycin-treated or serum-deprived conditions. This suggests that the antitumor effects of curcumin are influenced differently by curcumin-induced autophagy and the prerequisite basal level of autophagy in cancer cells.

• Biomolecules & Therapeutics
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• 제30권3호
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• pp.257-264
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• 2022

Colorectal cancer (CRC) is one of the most common malignant tumor. 5-FU is commonly used for the treatment of CRC. However, the development of drug resistance in tumor chemotherapy can seriously reduce therapeutic efficacy of 5-FU. Recent data show that FoxM1 is associated with 5-FU resistance in CRC. FoxM1 plays a critical role in the carcinogenesis and drug resistance of several malignancies. It has been reported that urushiol V isolated from the cortex of Rhus verniciflua Stokes is cytotoxic to several types of cancer cells. However, the underlying molecular mechanisms for its antitumor activity and its potential to attenuate the chemotherapeutic resistance in CRC cells remain unknown. Here, we found that urushiol V could inhibit the cell proliferation and induced S-phase arrest of SW480 colon cancer cells. It inhibited protein expression level of FoxM1 through activation of AMPK. We also investigated the combined effect of urushiol V and 5-FU. The combination treatment reduced FoxM1 expression and consequently reduced cell growth and colony formation in 5-FU resistant colon cancer cells (SW480/5-FUR). Taken together, these result suggest that urushiol V from Rhus verniciflua Stokes can suppress cell proliferation by inhibiting FoxM1 and enhance the antitumor capacity of 5-FU. Therefore, urushiol V may be a potential bioactive compound for CRC therapy.

• Bulletin of the Korean Chemical Society
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• 제35권5호
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• pp.1337-1342
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• 2014

A novel and convenient route for the synthesis of a series of thalidomide derivatives is described. Compound 2 was cyclized with different amines under alkaline condition to obtain 4-nitro substituted phthalimidines 3a-d. Hydroxylactams 4a-d were produced via bromination and hydroxylation. Different acyl chlorides were reacted with hydroxylactams to provide the desired esters 5a-d. All compounds were evaluated by MTT assay for their inhibitory activities against HCT-116, MG-63, MCF-7, HUVEC and HMVEC cell lines in vitro. Most of them showed no obvious cytotoxic effect on normal human cells, compounds 4a-d, $5a_2$, $5a_4$, $5a_5$, $5b_2$, $5c_2$ and $5d_2$ exhibited potent antitumor activities, among which compounds $5a_2$ and $5b_2$ were more effective than 5-FU.

• 대한의생명과학회지
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• 제19권4호
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• pp.303-309
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• 2013

Oncolytic vaccinia virus is an engineered vaccinia virus that selectively destroys cancer cells and induces tumor immune response. Oncolytic vaccinia expressing mouse GM-CSF showed cytotoxic activity against various kinds of cancer cells when oncolytic vaccinia virus expressing human GM-CSF and mouse GM-CSF is intravenously administered in the mouse CT26 colon tumor model. Cancer cells treated with isolated immunoglobulin G from the serum with complement showed these cytotoxic activity and complement observed dose-dependent cytotoxic effect. These results suggest that oncolytic vaccinia virus expressing mouse GM-CSF can increase oncolytic vaccinia virus by inducing anticancer antibody in a mouse tumor model. Further studies are needed on antitumor immunity of GM-CSF.

• Natural Product Sciences
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• 제8권2호
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• pp.52-54
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• 2002

The cultured mycelia of fungus Ganoderma lucidum were investigated for the inhibitory effect on the growth of s.c. transplanted Lewis lung carcinoma (LLC) in BDF-1 mice by intraperitoneal (i.p.) administration. The cultured mycelia showed antitumor activity with T/C values of 89.6 and 50.3 % at doses of 100 and 500 mg/kg, respectively, compared to adriamycin, which was used a positive control, with T/C value of 54.6 % at 2 mg/kg.

• 한국작물학회지
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• 제43권3호
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• pp.168-171
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• 1998

Sesaminol in sesame seed was postulated to have antitumor activity. The present study was performed to characterize the role of crude sesaminol extracted from sesame seed (Sesame Crude Sesaminol; SCS) on inhibiting the in vitro growth of human leukemia HL-60 cells. SCS inhibited the growth of human leukemia HL 60 cells in culture and macromolecular synthesis in a dose and time dependent manner. The cytostatic range of SCS concentration was found to be 60 to 100 $\mu\textrm{g}$/ml. SCS concentration greater than 200 $\mu\textrm{g}$/mlwere cytocidal to HL-60 cells. When SCS concentraction was 6 $\mu\textrm{g}$/mland 50 $\mu\textrm{g}$/ml the synthesis of HL-60 cells was inhibited by 35% for DNA, 6% for RNA and 5% for protein and 83% for DNA, 76% for RNA and 60% for protein. Of specific interest was the irreversible effect of SCS in inhibiting DNA synthesis of HL-60 cells. This was evidenced from the fact that, even after washed with PBS three times, preincubated HL-60 cells still showed the inhibited DNA synthesis.