• Title/Summary/Keyword: Liver cancer cell

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Inhibition of proliferation of human breast cancer cell (SK-BR3) and liver cancer cell(SK-Hepl) in tissue culture by the CCCA from Cordyceps militaris

  • Lee, Seung-Jeong;Han, Shin-Ha;Park, Eun-Jung;Lee, Chong-Kil;You, Byeong-Jin;Cho, Kyung-Hee;Ha, Nam-Joo;Kim, Kyung-Jae
    • Proceedings of the PSK Conference
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    • 2003.10b
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    • pp.140.1-140.1
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    • 2003
  • Permanent cell culture lines derived from human cancer tissue are important experimental models in the study of human cancer cell proliferation. The in vitro effects of C. militaris and its extracted fractions on the human breast cancer (SK-BR3), liver cancer (SK-Hep1, HepG2), kidney cancer (p15), lymphoma (Jurkat) were studied. F1 (CCCA, crude cordycepin containing adenosine), F2 (ethanol precipitation), F3 (ethanol soluble supernatant) and F4 (fraction of through SK-1B) significantly stimulated in vitro cytotoxic in human cancer cell lines. (omitted)

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PROM1-mediated cell signal transduction in cancer stem cells and hepatocytes

  • Myeong-Suk Bahn;Young-Gyu Ko
    • BMB Reports
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    • v.56 no.2
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    • pp.65-70
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    • 2023
  • Prominin-1 (PROM1), also called CD133, is a penta-span transmembrane protein that is localized in membrane protrusions, such as microvilli and filopodia. It is known to be expressed in cancer stem cells and various progenitor cells of bone marrow, liver, kidney, and intestine. Accumulating evidence has revealed that PROM1 has multiple functions in various organs, such as eye, tooth, peripheral nerve, and liver, associating with various molecular protein partners. PROM1 regulates PKA-induced gluconeogenesis, TGFβ-induced fibrosis, and IL-6-induced regeneration in the liver, associating with Radixin, SMAD7, and GP130, respectively. In addition, PROM1 is necessary to maintain cancer stem cell properties by activating PI3K and β-Catenin. PROM1-deficienct mice also show distinct phenotypes in eyes, brain, peripheral nerves, and tooth. Here, we discuss recent findings of PROM1-mediated signal transduction.

Effect of Broccoli Extract on Inhibition of Cancer Cell Proliferation (브로콜리 추출물의 암세포 증식 억제에 미치는 효과)

  • Jeong-Sook Park
    • Journal of Digital Policy
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    • v.2 no.1
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    • pp.31-35
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    • 2023
  • This study was conducted to examine the effect of Broccoli Extract on the proliferation inhibition of human-derived cancer cells and the degree of inhibition. The three cell lines used in the experiment were respiratory system lung cancer cells A549, digestive system liver cancer cells SNU-182 and biliary tract cancer SNU-1196. All cancer cells were derived from the human body, and the CCK-8 method was used to measure the degree of inhibition of cancer cell proliferation. As a result of examining the effect on Broccoli Extract 10ug/mL, 100ug/mL, 1000ug/mL, Broccoli Extract inhibited proliferation in a concentration-dependent manner in most cancer cells, In particular, lung cancer cell A549 and liver cancer cell SNU-182 showed significant proliferation inhibition at 1000ug/mL.As a result, it can be seen that broccoli extract provides potential as a cancer preventive and therapeutic agent for tumor suppression mechanisms proven through cell experiments.

A Case of Gastric Large Cell Neuroendocrine Carcinoma with Multiple Liver Metastasis Treated with Hepatic Artery Infusion Chemotherapy Followed by Surgery

  • Sung Bum Kim;Kook Hyun Kim;Tae Nyeun Kim
    • Journal of Digestive Cancer Research
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    • v.3 no.1
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    • pp.26-29
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    • 2015
  • A 73-year-old male visited our hospital with a complaint of general weakness. He underwent pyloric preserving pancreas-toduodenectomy due to ampullary cancer three years ago. Abdominal computed tomography scan at initial visit revealed multiple hepatic masses. A PET-CT scan showed multiple FDG uptakes at whole liver. He underwent hepatic artery infusion chemotherapy (HAIC) for five cycles. During the first cycle of HAIC, he developed gastric ulcer bleeding and endoscopic hemostasis was done successfully. Esophagogastroduodenoscopy after the 5th cycle of HAIC revealed ulcer scar at gastric angle. PET-CT scan at 12 months showed no FDG uptake at liver, but a focal FDG uptakes at stomach and peri-gastric lymph nodes were newly developed. Esophagogastroduodenoscopy revealed about 3 cm sized mass at gastric angle. He underwent surgery and pathologic examination revealed large cell neuroendocrine carcinoma. We report a case of gastric large cell neuroendocrine carcinoma with liver metastasis treated with HAIC followed by surgery.

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The High Expressed Serum Soluble Neural Cell Adhesion Molecule, a High Risk Factor Indicating Hepatic Encephalopathy in Hepatocelular Carcinoma Patients

  • Liu, Tian-Hua;Guo, Kun;Liu, Ri-Qiang;Zhang, Shu;Huang, Zhuo-Hui;Liu, Yin-Kun
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.8
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    • pp.3131-3135
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    • 2015
  • Objective: To investigate whether the expression of serum soluble neural cell adhesion molecule (sNCAM) is associated with hepatic encephalopathy (HE) in hepatocelular carcinoma (HCC) patients. Materials and Methods: The Oncomine Cancer Microarray database was used to determine the clinical relevance of NCAM expression in different kinds of human cancers. Sera from 75 HCC cases enrolled in this study were assessed for expression of sNCAM by enzyme linked immunosorbent assay (ELISA). Results: Dependent on the Oncomine Cancer Microarray database analysis, NCAM was down regulated in 10 different kinds of cancer, like bladder cancer, brain and central nervous system cancer, while up-regulated in lung cancer, uterine corpus leiomyoma and sarcoma, compared to normal groups. Puzzlingly, NCAM expression demonstrated no significant difference between normal and HCC groups. However, we found by quantitative ELISA that the level of sNCAM in sera from HCC patients with HE ($347.4{\pm}151.9ng/ml$) was significantly more up-regulated than that in HCC patients without HE ($260.3{\pm}104.2ng/ml$), the p-value being 0.008. sNCAM may be an important risk factor of HE in HCC patients, the correlation coefficients was 0.278 (P<0.05) on rank correlation analysis. Conclusions: This study highlights that up-regulated level of serum sNCAM is associated with HE in HCC patients and suggests that the high expression can be used as an indicator.

Studies on the Inhibitory Effect of Berberidis Ramulus to the Liver Cancer (소벽(小檗)의 간암 억제효과에 대한 연구)

  • Lee, Chung-Heon;Han, Hyo-Sang;Lee, Young-Jong
    • The Korea Journal of Herbology
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    • v.25 no.4
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    • pp.121-128
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    • 2010
  • Objectives : This study purposed to research the inhibitory effect of Berberidis Ramulus on the liver cancer. Methods : A total extract of Berberidis Ramulus decoction were prepared. Through the measurement of the cell proliferation, apoptosis, morphology and cytokine level from the extracts, the influence on HepG2 cell were compared. Results : Berberidis Ramulus extract significantly inhibited the proliferation, increased the apoptosis, decreased the TGF-${\beta}$ gene expression and the K-RAS gene expression, significantly increased the level of TNF-${\alpha}$ secretion and increased the rates of IFN-${\gamma}$ secretory cells. Conclusion : It is suggested that Berberidis Ramulus extract turned out to have anti-cancer effects on HepG2 cell.

Apoptotic Effects of Eugenol-loaded Nanoemulsions in Human Colon and Liver Cancer Cell Lines

  • Majeed, Hamid;Antoniou, John;Fang, Zhong
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.21
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    • pp.9159-9164
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    • 2014
  • Background: In this study eugenol (EU) loaded nanoemulsions (NEs) emulsified with modified starch were prepared and their apoptotic potential against liver and colon cancer cells was examined in comparison with bulk EU. Materials and Methods: We prepared stable EU loaded NEs whcih were characterized by dynamic light scattering, centrifugation and gas chromatography. Furthermore, cell viability was determined using MTT assay, and apoptosis and cell cycle analysess by flow cytometry. Results: HB8065 (liver) and HTB37 (colon) cells when treated with EU:CA NEs demonstrated greater apoptotic cells percentages as evidenced by microscopic images and flow cytometric evaluations. It was observed that EU and EU:CA NE induced apoptosis in both cell lines via reactive oxygen species (ROS) generation. Conclusions: The present study demonstrated that ROS plays a critical role in EU and EU:CA NE induced apoptosis in HB8065 and HTB37 cells. This is the first report on the antiproliferative mechanisms of EU loaded NE.

GATA2-Mediated Transcriptional Activation of Notch3 Promotes Pancreatic Cancer Liver Metastasis

  • Lin, Heng;Hu Peng;Zhang, Hongyu;Deng, Yong;Yang, Zhiqing;Zhang, Leida
    • Molecules and Cells
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    • v.45 no.5
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    • pp.329-342
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    • 2022
  • The liver is the predominant metastatic site for pancreatic cancer. However, the factors that determine the liver metastasis and the specific molecular mechanisms are still unclear. In this study, we used human pancreatic cancer cell line Hs766T to establish Hs766T-L3, a subline of Hs766T with stable liver metastatic ability. We performed RNA sequencing of Hs766T-L3 and its parental cell line Hs766T, and revealed huge differences in gene expression patterns and pathway activation between these two cell lines. We correlated the difference in pathway activation with the expression of the four core transcriptional factors including STAT1, NR2F2, GATA2, and SMAD4. Using the TCGA database, we examined the relative expression of these transcription factors (TFs) in pan-cancer and their relationship with the prognosis of the pancreatic cancer. Among these TFs, we considered GATA2 is closely involved in tumor metastasis and may serve as a potential metastatic driver. Further in vitro and in vivo experiments confirmed that GATA2-mediated transcriptional activation of Notch3 promotes the liver metastasis of Hs766T-L3, and knockdown of either GATA2 or Notch3 reduces the metastatic ability of Hs766T-L3. Therefore, we claim that GATA2 may serve as a metastatic driver of pancreatic cancer and a potential therapeutic target to treat liver metastasis of pancreatic cancer.

Inhibitory Effect of Beet Extract on Cancer Cell Proliferation (비트 추출물의 암세포 증식 저해 효과)

  • Lee, Jae-Hyeok;Park, Jeong-Sook
    • Journal of the Korea Convergence Society
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    • v.13 no.2
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    • pp.257-262
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    • 2022
  • The purpose of this study was to examine the inhibition of human cancer cell proliferation by using various concentrations of Beet Extract containing various bioactive ingredients. The six cancer cell lines used in the experiment were prostate cancer cells DU-145, lung cancer cells A549, breast cancer cells MCF-7, cervical cancer cells HeLa, liver cancer cells SNU-182, and biliary tract cancer cells SNU-1196. Human-derived cancer cell lines were used. The inhibition of cancer cell proliferation at various concentrations of Beet Extract was measured by the CCK-8 method. As a result of examining the inhibition of cancer cell proliferation, Beet Extract significantly and concentration-dependently inhibited DU145 of prostate cancer cells at all concentrations, and Lung cancer cells A549 and DU-145 of prostate cancer cells at 100ug/mL and 1000ug/mL, cervical cancer cells HeLa, and liver cancer cells SNU- 182, biliary tract cancer cell SNU-1196 showed significant proliferation inhibition at 1000ug/mL. Experiment result, the cancer cell proliferation inhibitory mechanisms of Beet Extract using various human-derived cancer cell lines can be considered to provide cancer prevention effects and the possibility of developing functional foods.

Inhibition of COX-2 Impairs Colon Cancer Liver Metastasis through Reduced Stromal Cell Reaction

  • Herrero, Alba;Benedicto, Aitor;Romayor, Irene;Olaso, Elvira;Arteta, Beatriz
    • Biomolecules & Therapeutics
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    • v.29 no.3
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    • pp.342-351
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    • 2021
  • Liver colonization is initiated through the interplay between tumor cells and adhesion molecules present in liver sinusoidal endothelial cells (LSECs). This crosstalk stimulates tumor COX-2 upregulation and PGE2 secretion. To elucidate the role of the LSEC intercellular adhesion molecule-1 (ICAM-1) in the prometastatic response exerted by tumor and stromal COX-2, we utilized celecoxib (CLX) as a COX-2 inhibitory agent. We analyzed the in vitro proliferative and secretory responses of murine C26 colorectal cancer (CRC) cells to soluble ICAM-1 (sICAM-1), cultured alone or with LSECs, and their effect on LSEC and hepatic stellate cell (HSC) migration and in vivo liver metastasis. CLX reduced sICAM-1-stimulated COX-2 activation and PGE2 secretion in C26 cells cultured alone or cocultured with LSECs. Moreover, CLX abrogated sICAM-1-induced C26 cell proliferation and C26 secretion of promigratory factors for LSECs and HSCs. Interestingly, CLX reduced the protumoral response of HSC, reducing their migratory potential when stimulated with C26 secretomes and impairing their secretion of chemotactic factors for LSECs and C26 cells and proliferative factors for C26 cells. In vivo, CLX abrogated the prometastatic ability of sICAM-1-activated C26 cells while reducing liver metastasis. COX-2 inhibition blocked the creation of a favorable tumor microenvironment (TME) by hindering the intratumoral recruitment of activated HSCs and macrophages in addition to the accumulation of fibrillar collagen. These results point to COX-2 being a key modulator of processes initiated by host ICAM-1 during tumor cell/LSEC/HSC crosstalk, leading to the creation of a prometastatic TME in the liver.