scholarly journals Methylglyoxal-Mediated Stress Correlates with High Metabolic Activity and Promotes Tumor Growth in Colorectal Cancer

2017 ◽  
Vol 18 (1) ◽  
pp. 213 ◽  
Author(s):  
Barbara Chiavarina ◽  
Marie-Julie Nokin ◽  
Justine Bellier ◽  
Florence Durieux ◽  
Noëlla Bletard ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Growth ◽  
Metabolic Activity ◽  
High Metabolic Activity

Pteridine and Riboflavin in Tumor Tissue and the Effect of Chloramphenicol and Isoxanthopterin

1972 ◽  
Vol 27 (3) ◽  
pp. 292-295 ◽  
Author(s):  
N. Kokolis ◽  
N. Mylonas ◽  
I. Ziegler
Keyword(s):  
Squamous Cell Carcinoma ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Metabolic Activity ◽  
Tumor Tissue ◽  
Mitotic Rate ◽  
Submaxillary Glands ◽  
Human Squamous Cell Carcinoma ◽  
Reduce Tumor Growth ◽  
High Metabolic Activity

Human squamous cell carcinoma has elevated levels of tetrahydrobiopterin. As the level of riboflavin is low, the ratio tetrahydrobiopterin/riboflavin shows values of 5 - 8.3. In contrast, in differentiated tissues with high metabolic activity but low mitotic rate, like submaxillary glands, elevated levels of tetrahydrobiopterin are accompanied by high content of riboflavin. Thus the ratio tetrahydrobiopterin/riboflavin in kept as low as about 0.5. Chloramphenicol and, in particular, isoxanthopterin reduce tumor growth in rats and prevent tetrahydrobiopterin accumulation as well.

Ultrastructural aspects of gymnosperms reproductive organs tissues due to their functional condition

1978 ◽  
Vol 36 (2) ◽  
pp. 440-441
Author(s):  
G. M. Kozubov
Keyword(s):  
Metabolic Activity ◽  
Functional Condition ◽  
Reproductive Organs ◽  
Considerable Change ◽  
Complicated Structure ◽  
Tetrad Stage ◽  
Ubisch Bodies ◽  
Similar Organization ◽  
Female Reproductive Organs ◽  
High Metabolic Activity

The ultrastructure of reproductive organs of pine, spruce, larch and ginkgo was investigated. It was found that the male reproductive organs possess similar organization. The most considerable change in the ultrastructure of the microsporocytes occur in meiosis. Sporoderm is being laid at the late tetrad stage. The cells of the male gameto-phyte are distinguished according to the metabolic activity of the or- ganells. They are most weakly developed in the spermiogenic cell. Ta-petum of the gymnosperms is of the periplasmodic - secretorial type. The Ubisch bodies which possess similar structure in the types investigated but are specific in details in different species are produced in tapetum.Parietal and subepidermal layers are distinguished for their high metabolic activity and are capable of the autonomous photosynthesis. Female reproductive organs differ more greatly in their struture and have the most complicated structure in primitive groups. On the first stages of their formation the inner cells of nucellus are transformed into the nucellar tapetum in which the structures similar to the Ubisch bodies taking part in the formation of the sporoderm of female gametophyte have been found.

scholarly journals RNF141 interacts with KRAS to promote colorectal cancer progression

Oncogene ◽  
2021 ◽  
Author(s):  
Jiuna Zhang ◽  
Xiaoyu Jiang ◽  
Jie Yin ◽  
Shiying Dou ◽  
Xiaoli Xie ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Plasma Membrane ◽  
Tumor Growth ◽  
Cancer Progression ◽  
Critical Role ◽  
Ring Finger ◽  
Immunohistochemical Analysis ◽  
Bimolecular Fluorescence Complementation

AbstractRING finger proteins (RNFs) play a critical role in cancer initiation and progression. RNF141 is a member of RNFs family; however, its clinical significance, roles, and mechanism in colorectal cancer (CRC) remain poorly understood. Here, we examined the expression of RNF141 in 64 pairs of CRC and adjacent normal tissues by real-time PCR, Western blot, and immunohistochemical analysis. We found that there was more expression of RNF141 in CRC tissue compared with its adjacent normal tissue and high RNF141 expression associated with T stage. In vivo and in vitro functional experiments were conducted and revealed the oncogenic role of RNF141 in CRC. RNF141 knockdown suppressed proliferation, arrested the cell cycle in the G1 phase, inhibited migration, invasion and HUVEC tube formation but promoted apoptosis, whereas RNF141 overexpression exerted the opposite effects in CRC cells. The subcutaneous xenograft models showed that RNF141 knockdown reduced tumor growth, but its overexpression promoted tumor growth. Mechanistically, liquid chromatography-tandem mass spectrometry indicated RNF141 interacted with KRAS, which was confirmed by Co-immunoprecipitation, Immunofluorescence assay. Further analysis with bimolecular fluorescence complementation (BiFC) and Glutathione-S-transferase (GST) pull-down assays showed that RNF141 could directly bind to KRAS. Importantly, the upregulation of RNF141 increased GTP-bound KRAS, but its knockdown resulted in a reduction accordingly. Next, we demonstrated that RNF141 induced KRAS activation via increasing its enrichment on the plasma membrane not altering total KRAS expression, which was facilitated by the interaction with LYPLA1. Moreover, KRAS silencing partially abolished the effect of RNF141 on cell proliferation and apoptosis. In addition, our findings presented that RNF141 functioned as an oncogene by upregulating KRAS activity in a manner of promoting KRAS enrichment on the plasma membrane in CRC.

scholarly journals Utidelone inhibits growth of colorectal cancer cells through ROS/JNK signaling pathway

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Fuli Li ◽  
Tinglei Huang ◽  
Yao Tang ◽  
Qingli Li ◽  
Jianzheng Wang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Growth ◽  
Xenograft Model ◽  
Jnk Pathway ◽  
Epothilone B ◽  
Colorectal Cancer Cells ◽  
M Phase ◽  
Jnk Signaling Pathway ◽  
Microtubule Stabilizing Agent

AbstractUtidelone (UTD1), a novel microtubule stabilizing agent, is an epothilone B analogue which was produced by genetic engineering. UTD1 has exhibited broad antitumor activity in multiple solid tumors. However, its activity and mechanism in colorectal cancer (CRC) remain to be studied. In this study, UTD1 dramatically inhibited CRC cell proliferation (with 0.38 µg/ml, 0.77 µg/ml IC50 in RKO and HCT116, respectively) in vitro. Immunofluorescence staining showed that UTD1 induced the formation of microtubule bundling and asters in RKO cells. Flow cytometry analysis demonstrated that UTD1 induced cell cycle to arrest in G2/M phase, subsequent apoptosis. Significantly, UTD1 exhibited stronger effect on inducing apoptosis than paclitaxel and 5-FU, especially in HCT15 cells which is ABCB1 high-expression. UTD1 exposure cleaved caspase-3 and poly ADP-ribose polymerase (PARP), decreased mitochondrial membrane potential, released cytochrome c, increased the production of active oxygen and activated c-Jun N-terminal kinase (JNK), suggesting ROS/JNK pathway was involved in this process. Moreover, UTD1 inhibited tumor growth and was more effective and safer compared with paclitaxel and 5-FU in RKO xenograft in nude mice. Taken together, our findings first indicate that UDT1 inhibits tumor growth in CRC xenograft model and may be a promising agent for CRC treatment.

scholarly journals Circular RNA circCSPP1 knockdown attenuates doxorubicin resistance and suppresses tumor progression of colorectal cancer via miR-944/FZD7 axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Lanlan Xi ◽  
Quanlin Liu ◽  
Wei Zhang ◽  
Linshan Luo ◽  
Jingfeng Song ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Growth ◽  
Circular Rna ◽  
Luciferase Reporter ◽  
Circular Rnas ◽  
Protein Levels ◽  
Cell Progression ◽  
Rna Immunoprecipitation ◽  
Induced Apoptosis

Abstract Background Circular RNAs (circRNAs) have been reported to play vital roles in colorectal cancer (CRC). However, only a few circRNAs have been experimentally validated and functionally described. In this research, we aimed to reveal the functional mechanism of circCSPP1 in CRC. Methods 36 DOX sensitive and 36 resistant CRC cases participated in this study. The expression of circCSPP1, miR-944 and FZD7 were detected by quantitative real time polymerase chain reaction (qRT-PCR) and the protein levels of FZD7, MRP1, P-gp and LRP were detected by western blot. Cell proliferation, migration, invasion, and apoptosis were assessed by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay, transwell assay, or flow cytometry analysis, respectively. The interaction between miR-944 and circCSPP1 or frizzled-7 (FZD7) was predicted by Starbase 3.0 and verified by the dual luciferase reporter assay, RNA immunoprecipitation (RIP) assay and RNA pull down assay. Xenograft tumor assay was performed to examine the effect of circCSPP1 on tumor growth in vivo. Results The expression of circCSPP1 and FZD7 was upregulated while miR-944 expression was downregulated in doxorubicin (DOX)-resistant CRC tissues and cells. CircCSPP1 knockdown significantly downregulated enhanced doxorubicin sensitivity, suppressed proliferation, migration, invasion, and induced apoptosis in DOX-resistant CRC cells. Interestingly, we found that circCSPP1 directly downregulated miR-944 expression and miR-944 decreased FZD7 level through targeting to 3′ untranslated region (UTR) of FZD7. Furthermore, circCSPP1 mediated DOX-resistant CRC cell progression and doxorubicin sensitivity by regulating miR-944/FZD7 axis. Besides, circCSPP1 downregulation dramatically repressed CRC tumor growth in vivo. Conclusion Our data indicated that circCSPP1 knockdown inhibited DOX-resistant CRC cell growth and enhanced doxorubicin sensitivity by miR-944/FZD7 axis, providing a potential target for CRC therapy.

scholarly journals LINC00963 affects the development of colorectal cancer via MiR-532-3p/HMGA2 axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jinjun Ye ◽  
Jidong Liu ◽  
Tao Tang ◽  
Le Xin ◽  
Xing Bao ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Growth ◽  
Cell Cycle Progression ◽  
Bioinformatics Analysis ◽  
Scratch Test ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Cycle Progression ◽  
Ki67 Expression ◽  
And Function

Abstract Background LINC00963 is high-expressed in various carcinomas, but its expression and function in colorectal cancer (CRC) have not been explored. This study explored the role and mechanism of LINC00963 in CRC. Methods The expression of LINC00963 in CRC and its relationship with prognosis were examined by starBase and survival analysis. The effects of LINC00963, miR-532-3p and HMGA2 on the biological characteristics and EMT-related genes of CRC cells were studied by RT-qPCR, CCK-8, clone formation experiments, flow cytometry, scratch test, Transwell, and Western blot. Xenograft assay and immunohistochemistry were performed to verify the effect of LINC00963 on tumor growth. The correlation among LINC00963, miR-532-3p, and HMGA2 was analyzed by bioinformatics analysis, luciferase assay, and Pearson test. Results LINC00963 was high-expressed in CRC, and this was associated with poor prognosis of CRC. Silencing LINC00963 inhibited the activity, proliferation, migration, and invasion of CRC cells, MMP-3 and MMP-9 expressions, moreover, it also blocked cell cycle progression, and inhibited tumor growth and Ki67 expression. However, overexpression of LINC00963 showed the opposite effects to silencing LINC00963. LINC00963 targeted miR-532-3p to regulate HMGA2 expression. Down-regulation of miR-532-3p promoted cell proliferation, migration and invasion, and expressions of MMP-3 and MMP-9, and knockdown of HMGA2 reversed the effect of miR-532-3p inhibitor. Up-regulation of miR-532-3p inhibited the biological functions of CRC cells, and overexpression of HMGA2 reversed the miR-532-3p mimic effect. Conclusion LINC00963 affects the development of CRC through the miR-532-3p/HMGA2 axis.

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