MiR-492 as an Important Biomarker for Early Diagnosis and Targeted Treatment in Different Cancers

2020 ◽  
Vol 16 (4) ◽  
pp. 269-275
Author(s):  
Eskandar Taghizadeh ◽  
Forough Taheri ◽  
Daryoush Rostami ◽  
Pedram G. Renani ◽  
Gordon A. Ferns ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Early Diagnosis ◽  
Cancer Colorectal ◽  
Human Cancer ◽  
Hepatocellular Cancer ◽  
Detailed Understanding ◽  
Human Cancer Cells ◽  
Cancer Initiation ◽  
Health And Disease ◽  
Potential Use

Recent studies have led to a more detailed understanding of the roles played by microRNAs in health and disease, and their potential use as biomarkers in physiological and pathophysiological processes involving cancer initiation and progression. MiR-492 is encoded by a pseudogene, has a key role in some human cancer cells and its overexpression in tissues, and it has been proposed that it can be used as a good biomarker for management and early diagnosis of some cancers including breast cancer, colorectal and ovarian cancer, hepatocellular cancer, retinoblastoma and pancreatic cancer. The aim of this review was to summarize the data of MiR-492 for early diagnosis and treatment of some types of related cancers.

scholarly journals New insights on CRISPR/Cas9-based therapy for breast Cancer

2021 ◽  
Vol 43 (1) ◽  
Author(s):  
Hussein Sabit ◽  
Shaimaa Abdel-Ghany ◽  
Huseyin Tombuloglu ◽  
Emre Cevik ◽  
Amany Alqosaibi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Research ◽  
Animal Models ◽  
Human Cancer ◽  
Step Process ◽  
Cancer Initiation ◽  
Malignant State ◽  
Treat Breast Cancer

AbstractCRISPR/Cas9 has revolutionized genome-editing techniques in various biological fields including human cancer research. Cancer is a multi-step process that encompasses the accumulation of mutations that result in the hallmark of the malignant state. The goal of cancer research is to identify these mutations and correlate them with the underlying tumorigenic process. Using CRISPR/Cas9 tool, specific mutations responsible for cancer initiation and/or progression could be corrected at least in animal models as a first step towards translational applications. In the present article, we review various novel strategies that employed CRISPR/Cas9 to treat breast cancer in both in vitro and in vivo systems.

Overexpression of ornithine decarboxylase enhances endothelial proliferation by suppressing endostatin expression

Blood ◽  
2002 ◽  
Vol 99 (4) ◽  
pp. 1478-1481 ◽  
Author(s):  
Takahiro Nemoto ◽  
Hisae Hori ◽  
Masataka Yoshimoto ◽  
Yousuke Seyama ◽  
Shunichiro Kubota
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Ornithine Decarboxylase ◽  
Human Cancer ◽  
Cos Cells ◽  
Human Cancer Cells ◽  
Collagen Expression ◽  
Endothelial Proliferation ◽  
Carboxyl Terminal

Angiogenesis, an essential process for tumor growth, is regulated by endothelial proliferation factors and their inhibitors such as endostatin. Endostatin, a carboxyl-terminal fragment of type XVIII collagen, inhibits endothelial proliferation, angiogenesis, and tumor growth. Ornithine decarboxylase (ODC), a molecule that is overexpressed in various cancers, is associated with promoting tumor growth and angiogenesis. We found that ODC-overexpressing human cancer cells and breast cancer specimens showed suppressed expression of type XVIII collagen and endostatin. We hypothesized that ODC overexpression may facilitate angiogenesis in tumors by suppressing endostatin expression. ODC-overexpressing COS cells, which showed suppressed type XVIII collagen and endostatin expression, were established. Conditioned media derived from these cells, containing decreased levels of endostatin, induced significant endothelial proliferation. ODC-overexpressing cells, when transplanted into nude mice, suppressed type XVIII collagen expression and promoted neovascularization in vivo. Thus, overexpression of ODC facilitates endothelial proliferation by suppressing endostatin expression.

scholarly journals Synthesis and anticancer activity of 5-sulfonyl derivatives of 1,3-oxazole-4-carboxylates

2020 ◽  
Vol 15 (2) ◽  
pp. 13-21
Author(s):  
Stepan Pilyo ◽  
Оlexandr Kozachenko ◽  
Victor Zhirnov ◽  
Maryna Kachaeva ◽  
Oleksandr Kobzar ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Molecular Docking ◽  
Complex Formation ◽  
Cancer Cells ◽  
Cell Lines ◽  
Human Cancer ◽  
Human Cancer Cells ◽  
Screening Protocol ◽  
Derivatives Of

A series of new 2-aryl 5-sulfonyl-1,3-oxazole-4-carboxylates for NCI anticancer screening protocol against 60 cancer cell lines were synthesized. Screening was performed in vitro on 60 cell lines of lungs, kidneys, CNS, ovaries, prostate, and breast cancer, leukemia, and melanoma. Methyl 5-benzylsulfonyl-2-phenyl-1,3-oxazole-4-carboxylate 15 exhibited potent and broad range of cytotoxic activity against tested human cancer cells with average GI50, TGI, and LC50 values of 5.37·10-6, 1.29·10-5 and 3.6·10-5 mol/L respectively. Molecular docking was used to evaluate the possible interaction of compound 15 with tubulin as well as a complex formation with CDK2.

scholarly journals The APOBEC3A deaminase drives episodic mutagenesis in cancer cells

2021 ◽  
Author(s):  
Mia Petljak ◽  
Kevan Chu ◽  
Alexandra Dananberg ◽  
Erik N. Bergstrom ◽  
Patrick von Morgen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Human Cancer ◽  
B Cell Lymphoma ◽  
Lymphoma Cell ◽  
Mutational Signatures ◽  
Cytidine Deaminases ◽  
Human Cancer Cells ◽  
Cancer Genomes

ABSTRACTThe APOBEC3 family of cytidine deaminases is widely speculated to be a major source of somatic mutations in cancer1–3. However, causal links between APOBEC3 enzymes and mutations in human cancer cells have not been established. The identity of the APOBEC3 paralog(s) that may act as prime drivers of mutagenesis and the mechanisms underlying different APOBEC3-associated mutational signatures are unknown. To directly investigate the roles of APOBEC3 enzymes in cancer mutagenesis, candidate APOBEC3 genes were deleted from cancer cell lines recently found to naturally generate APOBEC3-associated mutations in episodic bursts4. Deletion of the APOBEC3A paralog severely diminished the acquisition of mutations of speculative APOBEC3 origins in breast cancer and lymphoma cell lines. APOBEC3 mutational burdens were undiminished in APOBEC3B knockout cell lines. APOBEC3A deletion reduced the appearance of the clustered mutation types kataegis and omikli, which are frequently found in cancer genomes. The uracil glycosylase UNG and the translesion polymerase REV1 were found to play critical roles in the generation of mutations induced by APOBEC3A. These data represent the first evidence for a long-postulated hypothesis that APOBEC3 deaminases generate prevalent clustered and non-clustered mutational signatures in human cancer cells, identify APOBEC3A as a driver of episodic mutational bursts, and dissect the roles of the relevant enzymes in generating the associated mutations in breast cancer and B cell lymphoma cell lines.

scholarly journals Two isoleucyl tRNAs that decode ‘synonymous’ codons divergently regulate breast cancer progression

2021 ◽  
Author(s):  
Lisa B. Earnest-Noble ◽  
Dennis Hsu ◽  
Hosseinali Asgharian ◽  
Mandayam Nandan ◽  
Maria C. Passarelli ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Genome ◽  
Cancer Progression ◽  
Human Cancer ◽  
Breast Cancer Progression ◽  
Human Cancer Cells ◽  
Functional Studies ◽  
Synonymous Codons ◽  
Growth Promoting

The human genome contains 61 codons that encode for the 20 amino acids. The synonymous codons of a given amino acid are decoded by a set of transfer RNAs (tRNAs) called isoacceptors. We report the surprising observation that two isoacceptor tRNAs that decode synonymous codons are modulated in opposing directions during breast cancer progression. Specifically, tRNAIleUAU is upregulated, whereas tRNAIleGAU is repressed as breast cancer cells attained enhanced metastatic capacity. Functional studies revealed that tRNAIleUAU promoted and tRNAIleGAU suppressed metastatic colonization. The expression of these tRNAs mediated opposing effects on codon-dependent translation of growth promoting genes. Consistent with this, multiple mitotic gene sets in the human genome are significantly enriched in the codon cognate to the growth-promoting tRNAIleUAU and significantly depleted of the codon cognate to the growth-suppressive tRNAIleGAU. Our findings uncover a specific isoacceptor tRNA pair that act in opposition—divergently regulating genes that contribute to growth and a disease phenotype. The degeneracy of the genetic code can thus be biologically exploited by human cancer cells via tRNA isoacceptor shifts that facilitate the transition towards a growth-promoting state.

scholarly journals The APOBEC3A deaminase drives episodic mutagenesis in cancer cells

2021 ◽  
Author(s):  
John Maciejowski ◽  
Mia Petljak ◽  
Kevan Chu ◽  
Alexandra Dananberg ◽  
Erik Bergstrom ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Human Cancer ◽  
B Cell Lymphoma ◽  
Lymphoma Cell ◽  
Mutational Signatures ◽  
Cytidine Deaminases ◽  
Human Cancer Cells ◽  
Cancer Genomes

Abstract The APOBEC3 family of cytidine deaminases is widely speculated to be a major source of somatic mutations in cancer1–3. However, causal links between APOBEC3 enzymes and mutations in human cancer cells have not been established. The identity of the APOBEC3 paralog(s) that may act as prime drivers of mutagenesis and the mechanisms underlying different APOBEC3-associated mutational signatures are unknown. To directly investigate the roles of APOBEC3 enzymes in cancer mutagenesis, candidate APOBEC3 genes were deleted from cancer cell lines recently found to naturally generate APOBEC3-associated mutations in episodic bursts4. Deletion of the APOBEC3A paralog severely diminished the acquisition of mutations of speculative APOBEC3 origins in breast cancer and lymphoma cell lines. APOBEC3 mutational burdens were undiminished in APOBEC3B knockout cell lines. APOBEC3A deletion reduced the appearance of the clustered mutation types kataegis and omikli, which are frequently found in cancer genomes. The uracil glycosylase UNG and the translesion polymerase REV1 were found to play critical roles in the generation of mutations induced by APOBEC3A. These data represent the first evidence for a long-postulated hypothesis that APOBEC3 deaminases generate prevalent clustered and non-clustered mutational signatures in human cancer cells, identify APOBEC3A as a driver of episodic mutational bursts, and dissect the roles of the relevant enzymes in generating the associated mutations in breast cancer and B cell lymphoma cell lines.

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