Dual Roles for Epithelial Splicing Regulatory Proteins 1 (ESRP1) and 2 (ESRP2) in Cancer Progression

2016 ◽  
pp. 33-40 ◽  
Author(s):  
Akira Hayakawa ◽  
Masao Saitoh ◽  
Keiji Miyazawa
Keyword(s):  
Cancer Progression ◽  
Regulatory Proteins ◽  
Dual Roles

scholarly journals The Roles of Sirtuin Family Proteins in Cancer Progression

Cancers ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 1949 ◽  
Author(s):  
Erhu Zhao ◽  
Jianbing Hou ◽  
Xiaoxue Ke ◽  
Muhammad Nadeem Abbas ◽  
Saima Kausar ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Tumor Suppressors ◽  
Family Members ◽  
Critical Discussion ◽  
Biological Pathways ◽  
Tumor Promoters ◽  
Malignant Phenotype ◽  
Dual Roles ◽  
Adp Ribosyltransferase ◽  
High Degree

Sirtuin family members are characterized by either mono-ADP-ribosyltransferase or deacylase activity and are linked to various cancer-related biological pathways as regulators of transcriptional progression. Sirtuins play fundamental roles in carcinogenesis and maintenance of the malignant phenotype, mainly participating in cancer cell viability, apoptosis, metastasis, and tumorigenesis. Although sirtuin family members have a high degree of homology, they may play different roles in various kinds of cancer. This review highlights their fundamental roles in tumorigenesis and cancer development and provides a critical discussion of their dual roles in cancer, namely, as tumor promoters or tumor suppressors.

scholarly journals Lipid Regulatory Proteins as Potential Therapeutic Targets for Ovarian Cancer in Obese Women

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3469
Author(s):  
Jing Yang ◽  
M. Sharon Stack
Keyword(s):  
Ovarian Cancer ◽  
Cancer Progression ◽  
De Novo ◽  
Regulatory Element ◽  
Tumor Burden ◽  
Regulatory Proteins ◽  
De Novo Lipogenesis ◽  
Obese Women ◽  
Gynecological Malignancy ◽  
Global Epidemic

Obesity has become a recognized global epidemic that is associated with numerous comorbidities including type II diabetes, cardiovascular disease, hypertension, and cancer incidence and progression. Ovarian cancer (OvCa) has a unique mechanism of intra-peritoneal metastasis, already present in 80% of women at the time of diagnosis, making it the fifth leading cause of death from gynecological malignancy. Meta-analyses showed that obesity increases the risk of OvCa progression, leads to enhanced overall and organ-specific tumor burden, and adversely effects survival of women with OvCa. Recent data discovered that tumors grown in mice fed on a western diet (40% fat) have elevated lipid levels and a highly increased expression level of sterol regulatory element binding protein 1 (SREBP1). SREBP1 is a master transcription factor that regulates de novo lipogenesis and lipid homeostasis, and induces lipogenic reprogramming of tumor cells. Elevated SREBP1 levels are linked to cancer cell proliferation and metastasis. This review will summarize recent findings to provide a current understanding of lipid regulatory proteins in the ovarian tumor microenvironment with emphasis on SREBP1 expression in the obese host, the role of SREBP1 in cancer progression and metastasis, and potential therapeutic targeting of SREBPs and SREBP-pathway genes in treating cancers, particularly in the context of host obesity.

scholarly journals A role for the autophagic receptor, SQSTM1/p62, in trafficking NF-κB/RelA to nucleolar aggresomes

2020 ◽  
Author(s):  
Ian T Lobb ◽  
Pierre Morin ◽  
Kirsty Martin ◽  
Xhordi Lieshi ◽  
Karl Olsen ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Cancer Progression ◽  
Dominant Negative ◽  
Regulatory Proteins ◽  
Dominant Negative Mutant ◽  
Contributory Factor ◽  
Hallmarks Of Cancer ◽  
Solid Malignancies ◽  
Elevated Activity ◽  
Related Proteins

AbstractElevated NF-κB activity is a contributory factor in many haematological and solid malignancies. Nucleolar sequestration of NF-κB/RelA represses this elevated activity and mediates apoptosis of cancer cells. Here we set out to understand the mechanisms that control the nuclear/nucleolar distribution of RelA and other regulatory proteins, so that agents can be developed that specifically target these proteins to the organelle. We demonstrate that RelA accumulates in intra-nucleolar aggresomes in response to specific stresses. We also demonstrate that the autophagy receptor, SQSTM1/p62, accumulates alongside RelA in these nucleolar aggresomes. This accumulation is not a consequence of inhibited autophagy. Indeed, our data suggest nucleolar and autophagosomal accumulation of p62 are in active competition. We identify a conserved motif at the N-terminus of p62 that is essential for nucleoplasmic-to nucleolar transport of the protein. Furthermore, using a dominant negative mutant deleted for this nucleolar localisation signal (NoLS), we demonstrate a role for p62 in trafficking RelA and other aggresome-related proteins to nucleoli. Together, these data identify a novel role for p62 in trafficking nuclear proteins to nucleolar aggresomes under conditions of cell stress, thus maintaining nuclear proteostasis. They also provide invaluable information on the mechanisms that regulate the nuclear/nucleolar distribution of RelA that could be exploited for therapeutic purpose.SignificanceAberrant NF-κB activity drives many of the hallmarks of cancer and plays a key role in cancer progression. Nucleolar sequestration of NF-κB/RelA is one mechanism that switches off this activity and induces the death of cancer cells. Here we define a novel role for the autophagy receptor, SQSTM1/p62 in transport of nucleoplasmic NF-κB/RelA to nucleoli. Identification of this new trafficking mechanism opens up avenues for the development of a unique class of therapeutic agents that transport RelA and other cancer regulatory proteins to this organelle.

scholarly journals Molecular networks of FOXP family: dual biologic functions, interplay with other molecules and clinical implications in cancer progression

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Ju-Ha Kim ◽  
Jisung Hwang ◽  
Ji Hoon Jung ◽  
Hyo-Jung Lee ◽  
Dae Young Lee ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Cancer Progression ◽  
Noncoding Rnas ◽  
Treg Cells ◽  
Molecular Networks ◽  
Cellular Immunotherapy ◽  
Clinical Implications ◽  
Immune Disorders ◽  
Dual Roles ◽  
Forkhead Box

AbstractThough Forkhead box P (FOXP) transcription factors comprising of FOXP1, FOXP2, FOXP3 and FOXP4 are involved in the embryonic development, immune disorders and cancer progression, the underlying function of FOXP3 targeting CD4 + CD25+ regulatory T (Treg) cells and the dual roles of FOXP proteins as an oncogene or a tumor suppressor are unclear and controversial in cancers to date. Thus, the present review highlighted research history, dual roles of FOXP proteins as a tumor suppressor or an oncogene, their molecular networks with other proteins and noncoding RNAs, cellular immunotherapy targeting FOXP3, and clinical implications in cancer progression.

scholarly journals The role of collagen in cancer: from bench to bedside

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Shuaishuai Xu ◽  
Huaxiang Xu ◽  
Wenquan Wang ◽  
Shuo Li ◽  
Hao Li ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Signaling Pathways ◽  
Cancer Progression ◽  
Cell Activity ◽  
Dual Roles ◽  
Discoidin Domain Receptors ◽  
Other Substances ◽  
Tumor Cell Behavior ◽  
New Strategies

Abstract Collagen is the major component of the tumor microenvironment and participates in cancer fibrosis. Collagen biosynthesis can be regulated by cancer cells through mutated genes, transcription factors, signaling pathways and receptors; furthermore, collagen can influence tumor cell behavior through integrins, discoidin domain receptors, tyrosine kinase receptors, and some signaling pathways. Exosomes and microRNAs are closely associated with collagen in cancer. Hypoxia, which is common in collagen-rich conditions, intensifies cancer progression, and other substances in the extracellular matrix, such as fibronectin, hyaluronic acid, laminin, and matrix metalloproteinases, interact with collagen to influence cancer cell activity. Macrophages, lymphocytes, and fibroblasts play a role with collagen in cancer immunity and progression. Microscopic changes in collagen content within cancer cells and matrix cells and in other molecules ultimately contribute to the mutual feedback loop that influences prognosis, recurrence, and resistance in cancer. Nanoparticles, nanoplatforms, and nanoenzymes exhibit the expected gratifying properties. The pathophysiological functions of collagen in diverse cancers illustrate the dual roles of collagen and provide promising therapeutic options that can be readily translated from bench to bedside. The emerging understanding of the structural properties and functions of collagen in cancer will guide the development of new strategies for anticancer therapy.

scholarly journals SALL Proteins; Common and Antagonistic Roles in Cancer

Cancers ◽  
2021 ◽  
Vol 13 (24) ◽  
pp. 6292
Author(s):  
Claudia Álvarez ◽  
Aracelly Quiroz ◽  
Diego Benítez-Riquelme ◽  
Elizabeth Riffo ◽  
Ariel F. Castro ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cancer Progression ◽  
Cancer Biology ◽  
Genetic Disorders ◽  
Family Members ◽  
Tumor Development ◽  
Cancer Biomarkers ◽  
Regulatory Mechanisms ◽  
Dual Roles ◽  
Human Genetic Disorders

SALL proteins are a family of four conserved C2H2 zinc finger transcription factors that play critical roles in organogenesis during embryonic development. They regulate cell proliferation, survival, migration, and stemness; consequently, they are involved in various human genetic disorders and cancer. SALL4 is a well-recognized oncogene; however, SALL1–3 play dual roles depending on the cancer context and stage of the disease. Current reviews of SALLs have focused only on SALL2 or SALL4, lacking an integrated view of the SALL family members in cancer. Here, we update the recent advances of the SALL members in tumor development, cancer progression, and therapy, highlighting the synergistic and/or antagonistic functions they perform in similar cancer contexts. We identified common regulatory mechanisms, targets, and signaling pathways in breast, brain, liver, colon, blood, and HPV-related cancers. In addition, we discuss the potential of the SALL family members as cancer biomarkers and in the cancer cells’ response to therapies. Understanding SALL proteins’ function and relationship will open new cancer biology, clinical research, and therapy perspectives.

Toward an alignment of the actin molecule within the actin filament

1983 ◽  
Vol 41 ◽  
pp. 450-451
Author(s):  
P.R. Smith ◽  
W.E. Fowler ◽  
U. Aebi
Keyword(s):  
Actin Filament ◽  
Diffraction Data ◽  
Quantitative Estimate ◽  
Molecular Model ◽  
Quantitative Comparison ◽  
Regulatory Proteins ◽  
Essential Information ◽  
X Ray ◽  
Maximum Resolution ◽  
Lack Of Information

An understanding of the specific interactions of actin with regulatory proteins has been limited by the lack of information about the structure of the actin filament. Molecular actin has been studied in actin-DNase I complexes by single crystal X-ray analysis, to a resolution of about 0.6nm, and in the electron microscope where two dimensional actin sheets have been reconstructed to a maximum resolution of 1.5nm. While these studies have shown something of the structure of individual actin molecules, essential information about the orientation of actin in the filament is still unavailable.The work of Egelman & DeRosier has, however, suggested a method which could be used to provide an initial quantitative estimate of the orientation of actin within the filament. This method involves the quantitative comparison of computed diffraction data from single actin filaments with diffraction data derived from synthetic filaments constructed using the molecular model of actin as a building block. Their preliminary work was conducted using a model consisting of two juxtaposed spheres of equal size.

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