scholarly journals Characterization of the first microRNA in human CDH1 that affects cell cycle and apoptosis and indicates breast cancers progression

2022 ◽  
Author(s):  
Sedigheh Gharbi ◽  
Zahra Mohammadi ◽  
Maryam Saedi Dezaki ◽  
Sadat Dokanehiifard ◽  
Shahriar Dabiri ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Breast Cancers

scholarly journals Characterization of the Survival Influential Genes in Carcinogenesis

2021 ◽  
Vol 22 (9) ◽  
pp. 4384
Author(s):  
Divya Sahu ◽  
Yu-Lin Chang ◽  
Yin-Chen Lin ◽  
Chen-Ching Lin
Keyword(s):  
Cell Cycle ◽  
Cox Regression ◽  
Monte Carlo Algorithm ◽  
Functional Modules ◽  
Protective Genes ◽  
Cancer Types ◽  
Underlying Mechanisms ◽  
Patient Prognosis ◽  
Pan Cancer

The genes influencing cancer patient mortality have been studied by survival analysis for many years. However, most studies utilized them only to support their findings associated with patient prognosis: their roles in carcinogenesis have not yet been revealed. Herein, we applied an in silico approach, integrating the Cox regression model with effect size estimated by the Monte Carlo algorithm, to screen survival-influential genes in more than 6000 tumor samples across 16 cancer types. We observed that the survival-influential genes had cancer-dependent properties. Moreover, the functional modules formed by the harmful genes were consistently associated with cell cycle in 12 out of the 16 cancer types and pan-cancer, showing that dysregulation of the cell cycle could harm patient prognosis in cancer. The functional modules formed by the protective genes are more diverse in cancers; the most prevalent functions are relevant for immune response, implying that patients with different cancer types might develop different mechanisms against carcinogenesis. We also identified a harmful set of 10 genes, with potential as prognostic biomarkers in pan-cancer. Briefly, our results demonstrated that the survival-influential genes could reveal underlying mechanisms in carcinogenesis and might provide clues for developing therapeutic targets for cancers.

scholarly journals EARLY BUD-BREAK 1 and EARLY BUD-BREAK 3 control resumption of poplar growth after winter dormancy

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Abdul Azeez ◽  
Yiru Chen Zhao ◽  
Rajesh Kumar Singh ◽  
Yordan S. Yordanov ◽  
Madhumita Dash ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Molecular Mechanisms ◽  
Negative Regulator ◽  
Bud Break ◽  
Positive Regulator ◽  
Regulatory Module ◽  
Trees And Shrubs ◽  
Poplar Growth ◽  
Identification And Characterization

AbstractBud-break is an economically and environmentally important process in trees and shrubs from boreal and temperate latitudes, but its molecular mechanisms are poorly understood. Here, we show that two previously reported transcription factors, EARLY BUD BREAK 1 (EBB1) and SHORT VEGETATIVE PHASE-Like (SVL) directly interact to control bud-break. EBB1 is a positive regulator of bud-break, whereas SVL is a negative regulator of bud-break. EBB1 directly and negatively regulates SVL expression. We further report the identification and characterization of the EBB3 gene. EBB3 is a temperature-responsive, epigenetically-regulated, positive regulator of bud-break that provides a direct link to activation of the cell cycle during bud-break. EBB3 is an AP2/ERF transcription factor that positively and directly regulates CYCLIND3.1 gene. Our results reveal the architecture of a putative regulatory module that links temperature-mediated control of bud-break with activation of cell cycle.

scholarly journals Adenomatous Polyposis Coli Loss Controls Cell Cycle Regulators and Response to Paclitaxel

2020 ◽  
Author(s):  
Emily M. Astarita ◽  
Camden A. Hoover ◽  
Sara M. Maloney ◽  
T. Murlidharan Nair ◽  
Jenifer R. Prosperi
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Adenomatous Polyposis Coli ◽  
Cyclin B1 ◽  
Cell Cycle Analysis ◽  
Specific Cell ◽  
Breast Cancers ◽  
Cell Cycle Regulators ◽  
Adenomatous Polyposis ◽  
Polyposis Coli

AbstractAdenomatous Polyposis Coli (APC) is lost in approximately 70% of sporadic breast cancers, with an inclination towards triple negative breast cancer (TNBC). TNBC is treated with traditional chemotherapy, such as paclitaxel (PTX); however, tumors often develop drug resistance. We previously created APC knockdown cells (APC shRNA1) using the human TNBC cells, MDA-MB-157, and showed that APC loss induces PTX resistance. To understand the mechanisms behind APC-mediated PTX response, we performed cell cycle analysis and analyzed cell cycle related proteins. Cell cycle analysis indicated increased G2/M population in PTX-treated APC shRNA1 cells compared to PTX-treated controls, suggesting that APC expression does not alter PTX-induced G2/M arrest. We further studied the subcellular localization of the G2/M transition proteins, cyclin B1 and CDK1. The APC shRNA1 cells had increased CDK1, which was preferentially localized to the cytoplasm, and increased CDK6. RNA-sequencing was performed to gain a global understanding of changes downstream of APC loss and identified a broad mis-regulation of cell cycle-related genes in APC shRNA1 cells. Our studies are the first to show an interaction between APC and taxane response in breast cancer. The implications include designing combination therapy to re-sensitize APC-mutant breast cancers to taxanes using the specific cell cycle alterations.

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