scholarly journals Review of Natural Product-Derived Compounds as Potent Antiglioblastoma Drugs

2017 ◽  
Vol 2017 ◽  
pp. 1-24 ◽  
Author(s):  
Moon Nyeo Park ◽  
Hyo Sook Song ◽  
Myungsun Kim ◽  
Min-Jung Lee ◽  
Whisung Cho ◽  
...  
Keyword(s):  
Natural Products ◽  
Secretory Pathway ◽  
Suppressive Effect ◽  
Driver Mutations ◽  
Inhibitory Effects ◽  
Sargassum Serratifolium ◽  
Apoptosis Pathways ◽  
Key Driver ◽  
Related Pathway ◽  
Key Substances

Common care for glioblastoma multiforme (GBM) is a surgical resection followed by radiotherapy and temozolomide- (TMZ-) based chemotherapy. Unfortunately, these therapies remain inadequate involving severe mortality and recurrence. Recently, new approaches discovering combinations of multiple inhibitors have been proposed along with the identification of key driver mutations that are specific to each patient. To date, this approach is still limited by the lack of effective therapy. Hopefully, novel compounds derived from natural products are suggested as potential solutions. Inhibitory effects of natural products on angiogenesis and metastasis and cancer suppressive effect of altering miRNA expression are provident discoveries. Angelica sinensis accelerates apoptosis by their key substances influencing factors of apoptosis pathways. Brazilin displays antitumor features by making influence on reactive oxygen species (ROS) intensity. Sargassum serratifolium, flavonoids, and so on have antimetastasis effect. Ficus carica controls miRNA that inhibits translation of certain secretory pathway proteins during the UPR. Serratia marcescens and patupilone (EPO 906) are physically assessed materials through clinical trials related to GBM progression. Consequently, our review puts emphasis on the potential of natural products in GBM treatment by regulating multiple malignant cancer-related pathway solving pending problem such as reducing toxicity and side effect.

LEUKOCYTE MOTILITY: II. EFFECT OF ABSENCE OF GLUCOSE IN MEDIUM; EFFECT OF PRESENCE OF DEOXYGLUCOSE, DINITROPHENOL, PUROMYCIN, ACTINOMYCIN D, AND TRYPSIN ON THE RESPONSE TO CHEMOTACTIC SUBSTANCE; EFFECT OF SEGREGATION OF CELLS FROM CHEMOTACTIC SUBSTANCE

1967 ◽  
Vol 45 (2) ◽  
pp. 269-280 ◽  
Author(s):  
Bruce M. Carruthers
Keyword(s):  
Actinomycin D ◽  
Suppressive Effect ◽  
Inhibitory Effect ◽  
Medium Effect ◽  
Inhibitory Effects ◽  
In Vitro Motility ◽  
Directed Motility ◽  
A Minor ◽  
Chemotactic Effect

The random and directed motility of human leukocytes was studied in vitro. Motility was found not to be dependent upon glucose in the medium. 2-Deoxyglucose was found to inhibit all motility completely. Dinitrophenol had a minor suppressive effect on both random and directed motility. Puromycin at 10−3 M and actinomycin D at 10 μg/ml had a disproportionately great inhibitory effect on directed motility, when compared with minor inhibitory effects on random motility. Actinomycin D at 20 μg/ml and trypsin at 0.1 mg/ml were found to inhibit both types of motility almost completely. Segregation of starch from the field of leukocyte motility was found to abolish its chemotactic effect. Restoration of some chemotactic influence was seen if both starch and leukocytes were present in the segregated area.

scholarly journals The effects of mutational processes and selection on driver mutations across cancer types

2017 ◽  
Author(s):  
Daniel Temko ◽  
Ian PM Tomlinson ◽  
Simone Severini ◽  
Benjamin Schuster-Böckler ◽  
Trevor A Graham
Keyword(s):  
Driver Mutations ◽  
Sequencing Data ◽  
Epidemiological Evidence ◽  
Dna Mismatch ◽  
Cancer Types ◽  
Key Driver ◽  
Independent Effects ◽  
Mutational Processes ◽  
Mutation And Selection

ABSTRACTEpidemiological evidence has long associated environmental mutagens with increased cancer risk. However, links between specific mutation-causing processes and the acquisition of individual driver mutations have remained obscure. Here we have used public cancer sequencing data to infer the independent effects of mutation and selection on driver mutation complement. First, we detect associations between a range of mutational processes, including those linked to smoking, ageing, APOBEC and DNA mismatch repair (MMR) and the presence of key driver mutations across cancer types. Second, we quantify differential selection between well-known alternative driver mutations, including differences in selection between distinct mutant residues in the same gene. These results show that while mutational processes play a large role in determining which driver mutations are present in a cancer, the role of selection frequently dominates.

scholarly journals Natural products as modulators of eukaryotic protein secretion

2020 ◽  
Vol 37 (5) ◽  
pp. 717-736 ◽  
Author(s):  
Hendrik Luesch ◽  
Ville O. Paavilainen
Keyword(s):  
Natural Products ◽  
Protein Secretion ◽  
Secretory Pathway ◽  
Therapeutic Potential ◽  
Eukaryotic Protein ◽  
Mammalian Protein

This highlight reviews functions and therapeutic potential of diverse natural products that target different components of the mammalian protein secretory pathway.

scholarly journals Anti-tumor Promoting Activities of Natural Products. II. Inhibitory Effects of Digitoxin on Two-Stage Carcinogenesis of Mouse Skin Tumors and Mouse Pulmonary Tumors.

1993 ◽  
Vol 16 (9) ◽  
pp. 930-931 ◽  
Author(s):  
Akira INADA ◽  
Tsutomu NAKANISHI ◽  
Takao KONOSHIMA ◽  
Mutsuo KOZUKA ◽  
Harukuni TOKUDA ◽  
...  
Keyword(s):  
Natural Products ◽  
Mouse Skin ◽  
Skin Tumors ◽  
Inhibitory Effects ◽  
Two Stage ◽  
Pulmonary Tumors

scholarly journals Over expression of PTEN induces apoptosis and prevents cell proliferation in breast cancer cells

2020 ◽  
Author(s):  
Jinfeng Wu ◽  
Hong Gao ◽  
Wanyu Ge ◽  
Jie He
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Suppressive Effect ◽  
Logarithmic Growth Phase ◽  
Over Expression ◽  
Tensin Homolog ◽  
Apoptosis Pathways ◽  
And Migration

The phosphatase and tensin homolog (PTEN) is a tumor suppressor lipid phosphatase frequently mutated or deleted in breast cancer cells. Loss of PTEN is associated with aberrant activation of P13K/AKT signaling pathways, which are responsible for uncontrolled cell cycle, migration and prolonged survival. Therefore, stability and functional PTEN is essential for prevention of cancer growth and migration. In the present study, we have determined the effect of PTEN over expression in apoptosis induction and cell proliferation in breast cancer cells. We showed that PTEN over expression significantly declined the cell proliferation rate during logarithmic growth phase. Furthermore, the PTEN over expression leads to the activation of mitochondrial based intrinsic apoptosis pathways, which is confirmed by the activation and over expression of caspases 9 and caspases 3. In addition, the number of apoptotic cells are significantly more in PTEN over expressed cells, where they showed more apoptotic bodies in AO-EtBr and Hoechst 33344 staining. Finally, PTEN over expressed cells showed decreased chemo resistance as chemotherapeutic drugs kill them efficiently. Therefore, our findings suggest that tumor suppressive effect of PTEN is crucial for cancer prevention and thus PTEN might be a potential target for anti-cancer drugs.

scholarly journals Rpl24Bst mutation suppresses colorectal cancer by promoting eEF2 phosphorylation via eEF2K

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
John RP Knight ◽  
Nikola Vlahov ◽  
David M Gay ◽  
Rachel A Ridgway ◽  
William Liam Faller ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Protein Synthesis ◽  
Mouse Models ◽  
Mutant Mouse ◽  
Effective Means ◽  
Ribosomal Subunit ◽  
Suppressive Effect ◽  
Driver Mutations ◽  
Translation Elongation ◽  
Colorectal Tumorigenesis

Increased protein synthesis supports the rapid cell proliferation associated with cancer. The Rpl24Bst mutant mouse reduces the expression of the ribosomal protein RPL24 and has been used to suppress translation and limit tumorigenesis in multiple mouse models of cancer. Here, we show that Rpl24Bst also suppresses tumorigenesis and proliferation in a model of colorectal cancer (CRC) with two common patient mutations, Apc and Kras. In contrast to previous reports, Rpl24Bst mutation has no effect on ribosomal subunit abundance but suppresses translation elongation through phosphorylation of eEF2, reducing protein synthesis by 40% in tumour cells. Ablating eEF2 phosphorylation in Rpl24Bst mutant mice by inactivating its kinase, eEF2K, completely restores the rates of elongation and protein synthesis. Furthermore, eEF2K activity is required for the Rpl24Bst mutant to suppress tumorigenesis. This work demonstrates that elevation of eEF2 phosphorylation is an effective means to suppress colorectal tumorigenesis with two driver mutations. This positions translation elongation as a therapeutic target in CRC, as well as in other cancers where the Rpl24Bst mutation has a tumour suppressive effect in mouse models.

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