Proliferation Activity in Canine Gastrointestinal Lymphoma

The cellular uptake and lysosomal accumulation of 67Ga-labelled transferrin within tumors of different malignancy were examined using tissue fractionation and immunological techniques. As tumor models the slowly growing Morris hepatoma 5123C, the moderately growing Novikoff hepatoma and the fast and aggressive Yoshida hepatoma AH 130 were investigated. Isolation of subcellular fractions of tumor homogenates was performed by differential centrifugation and density-gradient centrifugation. The intracellular 67Gatransferrin was found to be highly concentrated within the purified lysosomes. The transferrin within the lysosomal fraction was identified by radial immunodiffusion technique using monospecific antiserum. The accumulation of 67Gatransferrin by the tumors resulted in a faster disappearance of 67Ga-transferrin from the blood. This loss of circulating 67Ga-transferrin correlated with the proliferation activity and the spread of the tumors. Since transferrin is indispensible for the utilization of iron by the heme-synthesizing red cell precursors, transferrin concentration in the blood is the limiting factor for the utilization of iron in hemoglobin synthesis. Thus, in a further series of experiments we investigated the development of anemia in tumor-bearing rats. With increasing tumor mass a progressive fall of hemoglobin concentration was found. The anemia was more severe in the faster growing Novikoff hepatoma than in the slowly growing Morris hepatoma. The most significant reduction of hemoglobin concentration was found in the very fast growing Yoshida hepatoma. After total tumor resection hemoglobin concentration and red blood cell count normalized completely within 6-8 weeks. We conclude from these data that the uptake of transferrin by the tumor cells results in a faster disappearance of transferrin from the blood. This loss of circulating transferrin correlates with tumor mass and proliferation activity and is one of the factors responsible for the anemia seen in patients with malignant tumors.

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Die Anämie bei malignen Tumorerkrankungen

Nuklearmedizin ◽

10.1055/s-0038-1629491 ◽

1989 ◽

Vol 28 (05) ◽

pp. 193-200 ◽

Cited By ~ 1

Author(s):

E. Aulbert

Keyword(s):

Cellular Uptake ◽

Tumor Tissue ◽

Malignant Tumors ◽

The Other ◽

Novikoff Hepatoma ◽

Cellular Accumulation ◽

Tumor Mass ◽

Proliferation Activity ◽

Morris Hepatoma ◽

Cellular Incorporation

Cellular uptake of 67Ga-labelled transferrin by the tumor tissue was studied in rats with tumors of different malignancy and different tumor mass using the slowly growing Morris hepatoma 5123C, the moderately growing Novikoff hepatoma and the very fast and aggressive Yoshida hepatoma AH130. The cellular accumulation of 67Ga-transferrin was found to correlate with the proliferation activity of the tumor. The 67Ga-transferrin concentration in the very fast growing Yoshida hepatoma was 4.8 times higher than the concentration in the slowly growing Morris hepatoma. The uptake of 67Ga-transferrin by the tumors resulted in a faster disappearance of circulating 67Ga-transferrin from the blood. The rate of disappearance correlated with the proliferation activity and the spread of the tumors. Using tumors of identical size the elimination of 67Ga-transferrin from the blood was much faster in the rats with Yoshida hepatoma than in those with the slowly growing Morris hepatoma. On the other hand, using tumors of different tumor size it could be demonstrated that the rate of disappearance of 67Ga-transferrin from the blood correlated directly with tumor mass. It is concluded that cellular incorporation of transferrin within the tumor cells results in a loss of circulating transferrin, which correlates with tumor mass and proliferation of tumor. This mechanism is supposed to be the cause for the hypotransferrinemia seen in patients with malignant tumors.

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The Effect of Crab Extract on the proliferation Activity of Colon Cancer Cell Line HCT-116

International Journal of Pharmaceutical Research ◽

10.31838/ijpr/2020.sp1.268 ◽

2020 ◽

Vol 12 (sp1) ◽

Keyword(s):

Colon Cancer ◽

Cell Line ◽

Cancer Cell ◽

Cancer Cell Line ◽

Colon Cancer Cell Line ◽

Colon Cancer Cell ◽

Proliferation Activity ◽

Hct 116

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Synergistic Roles of Curcumin in Sensitising the Cisplatin Effect on a Cancer Stem Cell-Like Population Derived from Non-Small Cell Lung Cancer Cell Lines

Molecules ◽

10.3390/molecules26041056 ◽

2021 ◽

Vol 26 (4) ◽

pp. 1056 ◽

Cited By ~ 1

Author(s):

Nazilah Abdul Satar ◽

Mohd Nazri Ismail ◽

Badrul Hisham Yahaya

Keyword(s):

Lung Cancer ◽

Stem Cell ◽

Small Cell Lung Cancer ◽

Cell Lung Cancer ◽

Cellular Proliferation ◽

Combined Treatment ◽

Small Cell ◽

Cytotoxic Agents ◽

Small Cell Lung ◽

Proliferation Activity

Cancer stem cells (CSCs) represent a small subpopulation within a tumour. These cells possess stem cell-like properties but also initiate resistance to cytotoxic agents, which contributes to cancer relapse. Natural compounds such as curcumin that contain high amounts of polyphenols can have a chemosensitivity effect that sensitises CSCs to cytotoxic agents such as cisplatin. This study was designed to investigate the efficacy of curcumin as a chemo-sensitiser in CSCs subpopulation of non-small cell lung cancer (NSCLC) using the lung cancer adenocarcinoma human alveolar basal epithelial cells A549 and H2170. The ability of curcumin to sensitise lung CSCs to cisplatin was determined by evaluating stemness characteristics, including proliferation activity, colony formation, and spheroid formation of cells treated with curcumin alone, cisplatin alone, or the combination of both at 24, 48, and 72 h. The mRNA level of genes involved in stemness was analysed using quantitative real-time polymerase chain reaction. Liquid chromatography-mass spectrometry was used to evaluate the effect of curcumin on the CSC niche. A combined treatment of A549 subpopulations with curcumin reduced cellular proliferation activity at all time points. Curcumin significantly (p < 0.001) suppressed colonies formation by 50% and shrank the spheroids in CSC subpopulations, indicating inhibition of their self-renewal capability. This effect also was manifested by the down-regulation of SOX2, NANOG, and KLF4. Curcumin also regulated the niche of CSCs by inhibiting chemoresistance proteins, aldehyde dehydrogenase, metastasis, angiogenesis, and proliferation of cancer-related proteins. These results show the potential of using curcumin as a therapeutic approach for targeting CSC subpopulations in non-small cell lung cancer.

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Gastrointestinal and oncologic outcomes of pediatric gastrointestinal lymphoma following upfront resection or biopsy of bowel masses

Pediatric Surgery International ◽

10.1007/s00383-021-04915-0 ◽

2021 ◽

Author(s):

Mohd Yusran Othman ◽

Huma Faiz Halepota ◽

Yun Le Linn ◽

York Tien Lee ◽

Kenneth T. E. Chang ◽

...

Keyword(s):

Oncologic Outcomes ◽

Gastrointestinal Lymphoma

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Sonic Hedgehog and Triiodothyronine Pathway Interact in Mouse Embryonic Neural Stem Cells

International Journal of Molecular Sciences ◽

10.3390/ijms21103672 ◽

2020 ◽

Vol 21 (10) ◽

pp. 3672

Author(s):

Pavel Ostasov ◽

Jan Tuma ◽

Pavel Pitule ◽

Jiri Moravec ◽

Zbynek Houdek ◽

...

Keyword(s):

Stem Cells ◽

Neural Stem Cells ◽

Sonic Hedgehog ◽

Shh Pathway ◽

Proliferation Activity ◽

The Central Nervous System ◽

Beta Gene ◽

Potential Tool ◽

Receptor Beta ◽

Transplantation Therapy

Neural stem cells are fundamental to development of the central nervous system (CNS)—as well as its plasticity and regeneration—and represent a potential tool for neuro transplantation therapy and research. This study is focused on examination of the proliferation dynamic and fate of embryonic neural stem cells (eNSCs) under differentiating conditions. In this work, we analyzed eNSCs differentiating alone and in the presence of sonic hedgehog (SHH) or triiodothyronine (T3) which play an important role in the development of the CNS. We found that inhibition of the SHH pathway and activation of the T3 pathway increased cellular health and survival of differentiating eNSCs. In addition, T3 was able to increase the expression of the gene for the receptor smoothened (Smo), which is part of the SHH signaling cascade, while SHH increased the expression of the T3 receptor beta gene (Thrb). This might be the reason why the combination of SHH and T3 increased the expression of the thyroxine 5-deiodinase type III gene (Dio3), which inhibits T3 activity, which in turn affects cellular health and proliferation activity of eNSCs.

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Isoflurane Regulates Proliferation, Apoptosis, and Inflammatory Response of Lipopolysaccharide-Induced Human Astrocyte through the miR-206/BDNF Axis

International Journal of Polymer Science ◽

10.1155/2020/8109294 ◽

2020 ◽

Vol 2020 ◽

pp. 1-8

Author(s):

Jianying Wang ◽

Zhiyuan Liu ◽

Xue Wang ◽

Yu Liu

Keyword(s):

Inflammatory Response ◽

Western Blotting ◽

Annexin V ◽

Luciferase Reporter ◽

Bdnf Expression ◽

Human Astrocyte ◽

Human Astrocytes ◽

Proliferation And Apoptosis ◽

Proliferation Activity ◽

Normal Human

Objective. To investigate the effect of isoflurane (ISO) on the proliferation, apoptosis, and inflammatory response of lipopolysaccharide- (LPS-) induced normal human astrocytes (NHAs) by regulating the miR-206/BDNF axis. Methods. NHA proliferation activity was measured by MTT; NHA apoptotic rates were measured by Annexin V-FITC/PI; western blotting was used to measure the BDNF expression; ELISA was used to measure the IL-6, IL-1β, and TNF-α expression in NHAs; qPCR was used to measure the expressions of miRNAs that are related to NHAs proliferation and apoptosis; dual-luciferase reporter was constructed to validate the targeting relationship between miR-206 and BDNF. Results. LPS increased the proliferation activity and decreased the apoptosis rate of NHAs which were effectively reversed by the ISO (p<0.05); LPS significantly inhibited the expression of miRNAs related to proliferation and apoptosis in NHAs (p<0.05, p<0.01), whereas ISO significantly increased the expression of miR-206 (p<0.01) by downregulating the expression of BDNF, thus inhibiting NHA proliferation and inflammatory response and enhancing apoptosis. Conclusion. ISO can inhibit the expression of BDNF by upregulating the expression of miR-206, thereby inhibiting the proliferation and inflammatory response of NHAs and promoting its apoptosis.

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