• 제목/요약/키워드: Cancer biology

검색결과 2,299건 처리시간 0.041초

Posttranscriptional deregulation of Src due to aberrant miR34a and miR203 contributes to gastric cancer development

  • Hao, Qiang;Lu, Xiaozhao;Liu, Nannan;Xue, Xiaochang;Li, Meng;Zhang, Cun;Qin, Xin;Li, Weina;Shu, Zhen;Song, Bin;Wang, Qing;Song, Liqiang;Zhang, Wei;Zhang, Yingqi
    • BMB Reports
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    • 제46권6호
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    • pp.316-321
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    • 2013
  • Gastric cancer remains the main cause of cancer death all around the world, and upregulated activation of the nonreceptor tyrosine kinase c-SRC (SRC) is a key player in the development. In this study, we found that expression of Src is also increased in clinical gastric cancer samples, with the protein level increased more significantly than that at the RNA level. Further study revealed that miR34a and miR203, two tumor suppressive miRNAs, inversely correlate with the expression of Src. Restoration of miR34a and miR203 decreased Src expression in gastric cancer cell lines, which in turn inhibited cell growth and cell migration. In summary, our study here revealed that posttranscriptional regulation of Src contributes to the deregulated cell growth and metastasis in gastric cancer, and targeting Src by miR34a or miR203 mimics would be a promising strategy in therapy.

MSP58 Knockdown Inhibits the Proliferation of Esophageal Squamous Cell Carcinoma in Vitro and in Vivo

  • Xu, Chun-Sheng;Zheng, Jian-Yong;Zhang, Hai-Long;Zhao, Hua-Dong;Zhang, Jing;Wu, Guo-Qiang;Wu, Lin;Wang, Qing;Wang, Wei-Zhong;Zhang, Jian
    • Asian Pacific Journal of Cancer Prevention
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    • 제13권7호
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    • pp.3233-3238
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    • 2012
  • Esophageal carcinoma (EC) is one of the most aggressive cancers with a poor prognosis. Understanding the molecular mechanisms underlying esophageal cancer progression is a high priority for improved EC diagnosis and prognosis. Recently, MSP58 was shown to behave as an oncogene in colorectal carcinomas and gliomas. However, little is known about its function in esophageal carcinomas. We therefore examined the effects of MSP58 knockdown on the growth of esophageal squamous cell carcinoma (ESCC) cells in vitro and in vivo in order to gain a better understanding of its potential as a tumor therapeutic target. We employed lentiviral-mediated small hairpin RNA (shRNA) to knock down the expression of MSP58 in the ESCC cell lines Eca-109 and EC9706 and demonstrated inhibition of ESCC cell proliferation and colony formation in vitro. Furthermore, flow cytometry and western blot analyses revealed that MSP58 depletion induced cell cycle arrest by regulating the expression of P21, CDK4 and cyclin D1. Notably, the downregulation of MSP58 significantly inhibited the growth of ESCC xenografts in nude mice. Our results suggest that MSP58 may play an important role in ESCC progression.

E1/E2 of Hepatitis C Virus Genotype-4 and Apoptosis

  • Zekri, Abdel-Rahman N;Sobhy, Esraa;Hussein, Nehal;Ahmed, Ola S;Hussein, Amira;Shoman, Sahar;Soliman, Amira H;El-Din, Hanaa M Alam
    • Asian Pacific Journal of Cancer Prevention
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    • 제17권7호
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    • pp.3131-3138
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    • 2016
  • Several studies have addressed the possible role of hepatitis C virus genotype-4 (HCV GT4) in apoptosis. However, this still not fully understood. In the current study a re-constructed clone of E1/E2 polyprotein region of the HCV GT4 was transfected into the Huh7 cell line and a human apoptotic PCR array of 84 genes was used to investigate its possible significance for apoptosis. Out of the 84 genes, only 35 showed significant differential expression, 12 genes being up-regulated and 23 down-regulated. The highest-up regulated genes were APAF1 (apoptotic peptidase-activating factor 1), BID (BH3 interacting domain death agonist) and BCL 10 (B-cell CLL/lymphoma protein 10) with fold regulation of 33.2, 30.1 and 18.9, respectively. The most down-regulated were FAS (TNF receptor super family), TNFRSF10B (tumor necrosis factor receptor super-family member 10b) and FADD (FAS-associated death domain) with fold regulation of -30.2, -27.7 and -14.9, respectively. These results suggest that the E1/E2 proteins may be involved in HCV-induced pathogenesis by modulating apoptosis through the induction of the intrinsic apoptosis pathway and disruption of the BCL2 gene family.

Anti-proliferation Effect of Damina 909 on Pancreatic Cancer Cells in Tumor-Xenografted Nude Mice Model

  • Kim, Yu-Ri;Lee, Seung-Min;Seo, Sang-Hui;Lee, Seung-Ho;Kim, In-Kyoung;Jun, Hwang-Jeok;Nam, Jong-Hyun;Kim, Meyoung-Kon
    • Molecular & Cellular Toxicology
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    • 제5권1호
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    • pp.7-13
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    • 2009
  • In this study, we investigated the anti-proliferative effect of Damina 909 in human cancer cell lines and tumor-xenografted nude mice to elucidate its potential in treating many cancers. Damina 909 treatment resulted in inhibition of cell proliferation of human pancreatic cancer cells. Our in vivo study showed that the weight of pancreatic tumors in Damina 909-treated group were the lighter than control group. Consequently, the intake of food and water in Damina 909-treated group did not change, while those in control group were steadily decreased over a period of treatment. Moreover, Damina 909 treatment elevated the protein expression of p53 and p21 in pancreatic tumor of xenografted nude mice. In summary, compare to other human cancer cells such as prostate and hepatocyte, Damina 909 is most effectively inhibited proliferation of pancreatic cancer cells by increasing the expression of tumor suppressor genes. This led us to speculate that a candidate substance for effective cancer therapy of pancreatic cancer might be contained in Damina 909.

Transcriptional Heterogeneity of Cellular Senescence in Cancer

  • Junaid, Muhammad;Lee, Aejin;Kim, Jaehyung;Park, Tae Jun;Lim, Su Bin
    • Molecules and Cells
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    • 제45권9호
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    • pp.610-619
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    • 2022
  • Cellular senescence plays a paradoxical role in tumorigenesis through the expression of diverse senescence-associated (SA) secretory phenotypes (SASPs). The heterogeneity of SA gene expression in cancer cells not only promotes cancer stemness but also protects these cells from chemotherapy. Despite the potential correlation between cancer and SA biomarkers, many transcriptional changes across distinct cell populations remain largely unknown. During the past decade, single-cell RNA sequencing (scRNA-seq) technologies have emerged as powerful experimental and analytical tools to dissect such diverse senescence-derived transcriptional changes. Here, we review the recent sequencing efforts that successfully characterized scRNA-seq data obtained from diverse cancer cells and elucidated the role of senescent cells in tumor malignancy. We further highlight the functional implications of SA genes expressed specifically in cancer and stromal cell populations in the tumor microenvironment. Translational research leveraging scRNA-seq profiling of SA genes will facilitate the identification of novel expression patterns underlying cancer susceptibility, providing new therapeutic opportunities in the era of precision medicine.

Influence of Tyrosol on Cell Growth Inhibition of KB Human Oral Cancer Cells

  • Lee, Ue-Kyung;Kim, Su-Gwan;Go, Dae-San;Yu, Sun-Kyoung;Kim, Chun Sung;Kim, Jeongsun;Kim, Do Kyung
    • International Journal of Oral Biology
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    • 제41권4호
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    • pp.175-181
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    • 2016
  • Tyrosol, a phenylethanoid and a derivative of phenethyl alcohol, possesses various biological properties, such as anti-oxidative and cardioprotective activity. Olive oil is the principal source of tyrosol in the human diet. However, so far the anti-cancer activity of tyrosol has not yet been well defined. This study therefore undertakes to examine the cytotoxic activity and the mechanism of cell death exhibited by tyrosol in KB human oral cancer cells. Treatment of KB cells with tyrosol induced the cell growth inhibition in a concentration- and a time-dependent manner. Furthermore, the treatment of tyrosol induced nuclear condensation and fragmentation of KB cells. Tyrosol also promoted proteolytic cleavage of procaspase-3, -7, -8 and -9, increasing the amounts of cleaved caspase-3, -7, -8 and -9. In addition, tyrosol increased the levels of cleaved PARP in KB cells. These results suggest that tyrosol induces the suppression of cell growth and cell apoptosis in KB human oral cancer cells, and is therefore a potential candidate for anti-cancer drug discovery.

The Cancer Stem Cell Theory: Is It Correct?

  • Yoo, Min-Hyuk;Hatfield, Dolph L.
    • Molecules and Cells
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    • 제26권5호
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    • pp.514-516
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    • 2008
  • The cancer stem cell hypothesis posits that tumor growth is driven by a rare subpopulation of cells, designated cancer stem cells (CSC). Studies supporting this theory are based in large part on xenotransplantation experiments wherein human cancer cells are grown in immunocompromised mice and only CSC, often constituting less than 1% of the malignancy, generate tumors. Herein, we show that all colonies derived from randomly chosen single cells in mouse lung and breast cancer cell lines form tumors following allografting histocompatible mice. Our study suggests that the majority of malignant cells rather than CSC can sustain tumors and that the cancer stem cell theory must be reevaluated.

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
    • 대한약학회:학술대회논문집
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    • 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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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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New established cell lines from undifferentiated pleomorphic sarcoma for in vivo study

  • Eun-Young Lee;Young-Ho Kim;Md Abu Rayhan;Hyun Guy Kang;June Hyuk Kim;Jong Woong Park;Seog-Yun Park;So Hee Lee;Hye Jin You
    • BMB Reports
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    • 제56권4호
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    • pp.258-264
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    • 2023
  • As a high-grade soft-tissue sarcoma (STS), undifferentiated pleomorphic sarcoma (UPS) is highly recurrent and malignant. UPS is categorized as a tumor of uncertain differentiation and has few options for treatment due to its lack of targetable genetic alterations. There are also few cell lines that provide a representative model for UPS, leading to a dearth of experimental research. Here, we established and characterized new cell lines derived from two recurrent UPS tissues. Cells were obtained from UPS tissues by mincing, followed by extraction or dissociation using enzymes and culture in a standard culture environment. Cells were maintained for several months without artificial treatment, and some cell clones were found to be tumorigenic in an immunodeficient mouse model. Interestingly, some cells formed tumors in vivo when injected after aggregation in a non-adherent culture system for 24 h. The tissues from in vivo study and tissues from patients shared common histological characteristics. Pathways related to the cell cycle, such as DNA replication, were enriched in both cell clones. Pathways related to cell-cell adhesion and cell-cell signaling were also enriched, suggesting a role of the mesenchymal-to-epithelial transition for tumorigenicity in vivo. These new UPS cell lines may facilitate research to identify therapeutic strategies for UPS.