scholarly journals An overview of the perspective of cellular autophagy: Mechanism, regulation, and the role of autophagy dysregulation in the pathogenesis of diseases

2021 ◽  
Vol 0 (0) ◽  
pp. 0
Author(s):  
AymanZ Elsamanoudy ◽  
YasserM Alharbi ◽  
AbdulhadiI Bima
Keyword(s):  
Cellular Autophagy

scholarly journals Multiple Roles of Autophagy in the Sorafenib Resistance of Hepatocellular Carcinoma

2017 ◽  
Vol 44 (2) ◽  
pp. 716-727 ◽  
Author(s):  
Ting Sun ◽  
Hongchun Liu ◽  
Liang Ming
Keyword(s):  
Hepatocellular Carcinoma ◽  
Current Knowledge ◽  
Acquired Resistance ◽  
Multiple Roles ◽  
Multikinase Inhibitor ◽  
Advanced Hcc ◽  
Cellular Autophagy ◽  
Advanced Stages ◽  
Hcc Cells

Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related death worldwide, and prognosis remains unsatisfactory since the disease is often diagnosed at the advanced stages. Currently, the multikinase inhibitor sorafenib is the only drug approved for the treatment of advanced HCC. However, primary or acquired resistance to sorafenib develops, generating a roadblock in HCC therapy. Autophagy is an intracellular lysosomal pathway involved in protein and organelle degradation, with an astonishing number of connections to human disease and physiology. Current understanding of the role of autophagy in the progression of cancer and the response to cancer therapy remains controversial. Sorafenib is able to induce autophagy in HCC, but the effect of autophagy is indistinct. Some studies established that sorafenib-induced autophagy serves as a pro-survival response. However, other studies found that sorafenib-induced autophagy improves the lethality of sorafenib against HCC cells. The mechanisms underlying autophagy and sorafenib resistance remain elusive. The purpose of this review is to summarize the progress of research focused on autophagy and sorafenib resistance and to update current knowledge of how cellular autophagy impacts sorafenib sensitivity in HCC treatment.

scholarly journals Rottlerin Reduces cAMP/CREB-Mediated Melanogenesis via Regulation of Autophagy

2019 ◽  
Vol 20 (9) ◽  
pp. 2081 ◽  
Author(s):  
Nurinanda Prisky Qomaladewi ◽  
Mi-Yeon Kim ◽  
Jae Youl Cho
Keyword(s):  
Signaling Pathway ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Camp Response Element Binding ◽  
Sequential Process ◽  
Camp Response Element ◽  
Melanin Production ◽  
Melanocyte Stimulating Hormone ◽  
Cellular Autophagy

Melanogenesis is the sequential process of melanin production by melanocytes in order to protect the skin from harmful stimuli. Melanogenesis is disrupted by radiation exposure, which results in the differentiation of melanocytes into melanoma. Recently, some methods have been developed to maintain the instability of melanogenesis in melanoma by activating cellular autophagy. However, there is still a lack of knowledge about how autophagy is involved in the regulation of melanogenesis in melanoma cells. Here, we used rottlerin as an autophagy inducer to investigate the role of the cyclic adenosine monophosphate (cAMP)/cAMP response element binding (CREB) signaling pathway in melanogenesis. We found that rottlerin can inhibit melanin production by targeting cAMP, which is initially activated by alpha-melanocyte stimulating hormone (α-MSH). Our findings suggest that rottlerin has a pivotal role as an autophagy inducer in the regulation of melanogenesis by targeting the cAMP/CREB signaling pathway.

scholarly journals Role of Microtubules in Extracellular Release of Poliovirus

2009 ◽  
Vol 83 (13) ◽  
pp. 6599-6609 ◽  
Author(s):  
Matthew P. Taylor ◽  
Trever B. Burgon ◽  
Karla Kirkegaard ◽  
William T. Jackson
Keyword(s):  
Secretory Pathway ◽  
Infectious Agents ◽  
Wild Type ◽  
Macromolecular Complexes ◽  
Extracellular Virus ◽  
Cellular Autophagy ◽  
Extracellular Release ◽  
Vesicle Movement ◽  
Cellular Lysis

ABSTRACT Cellular autophagy, a process that directs cytosolic contents to the endosomal and lysosomal pathways via the formation of double-membraned vesicles, is a crucial aspect of innate immunity to many intracellular pathogens. However, evidence is accumulating that certain RNA viruses, such as poliovirus, subvert this pathway to facilitate viral growth. The autophagosome-like membranes induced during infection with wild-type poliovirus were found to be, unlike cellular autophagosomes, relatively immobile. Their mobility increased upon nocodazole treatment, arguing that vesicular tethering is microtubule dependent. In cells infected with a mutant virus that is defective in its interaction with the host cytoskeleton and secretory pathway, vesicle movement increased, indicating reduced tethering. In all cases, the release of tethering correlated with increased amounts of extracellular virus, which is consistent with the hypothesis that small amounts of cytosol and virus entrapped by double-membraned structures could be released via fusion with the plasma membrane. We propose that this extracellular delivery of cytoplasmic contents be termed autophagosome-mediated exit without lysis (AWOL). This pathway could explain the observed exit, in the apparent absence of cellular lysis, of other cytoplasmic macromolecular complexes, including infectious agents and complexes of aggregated proteins.

scholarly journals Molecular Insights into the Multifunctional Role of Natural Compounds: Autophagy Modulation and Cancer Prevention

2020 ◽  
Author(s):  
Md. Ataur Rahman ◽  
Hasanur Rahman ◽  
Md. Shahadat Hossain ◽  
Partha Biswas ◽  
Rokibul Islam ◽  
...  
Keyword(s):  
Side Effects ◽  
Cancer Treatment ◽  
Cancer Prevention ◽  
Stress Responses ◽  
Natural Compounds ◽  
Degradation Pathway ◽  
Synthetic Chemicals ◽  
Cellular Autophagy ◽  
Autophagy Pathway

Autophagy is a vacuolar, lysosomal degradation pathway for injured and damaged protein molecules and organelles in eukaryotic cells, which is controlled by nutrients and stress responses. Dysregulation of cellular autophagy may lead to various diseases such as neurodegenerative disease, obesity, cardiovascular disease, diabetes, and malignancy. Recently, natural compounds have come to attention for being able to modulate the autophagy pathway in cancer prevention, although the prospective role of autophagy in cancer treatment is very complex and not yet clearly elucidated. Numerous synthetic chemicals have been identified that modulate autophagy and are favorable candidates for cancer treatment, but they have adverse side effects. Therefore, different phytochemicals, which include natural compounds and their derivatives, have attracted significant attention for use as autophagy modulators in cancer treatment with minimal side effects. In the current review, we discuss the promising role of natural compounds in modulating the autophagy pathway to control and prevent cancer, and provide possible therapeutic options.

scholarly journals MicroRNA-205-5p inhibits skin cancer cell proliferation and increase drug sensitivity by targeting TNFAIP8

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xinhong Ge ◽  
Suryakant Niture ◽  
Minghui Lin ◽  
Patrice Cagle ◽  
P. Andy Li ◽  
...  
Keyword(s):  
Skin Cancer ◽  
Cell Carcinoma ◽  
Kinase Inhibitor ◽  
Ectopic Expression ◽  
Cancer Cell Proliferation ◽  
Growth And Survival ◽  
Cellular Autophagy ◽  
Increased Sensitivity ◽  
Factor Α

AbstractTumor necrosis factor-α-induced protein 8 (TNFAIP8) is a member of the TIPE/TNFAIP8 family which regulates tumor growth and survival. Our goal is to delineate the detailed oncogenic role of TNFAIP8 in skin cancer development and progression. Here we demonstrated that higher expression of TNFAIP8 is associated with basal cell carcinoma (BCC), squamous cell carcinoma (SCC), and melanoma development in patient tissues. Induction of TNFAIP8 expression by TNFα or by ectopic expression of TNFAIP8 in SCC or melanoma cell lines resulted in increased cell growth/proliferation. Conversely, silencing of TNFAIP8 decreased cell survival/cell migration in skin cancer cells. We also showed that miR-205-5p targets the 3′UTR of TNFAIP8 and inhibits TNFAIP8 expression. Moreover, miR-205-5p downregulates TNFAIP8 mediated cellular autophagy, increased sensitivity towards the B-RAFV600E mutant kinase inhibitor vemurafenib, and induced cell apoptosis in melanoma cells. Collectively our data indicate that miR-205-5p acts as a tumor suppressor in skin cancer by targeting TNFAIP8.

Morphometric Analysis of Particulate Fractions from Rat Liver

1970 ◽  
Vol 28 ◽  
pp. 76-77
Author(s):  
Russel L. Deter
Keyword(s):  
Rat Liver ◽  
Morphometric Analysis ◽  
Quantitative Information ◽  
Small Samples ◽  
Morphological Evaluation ◽  
Cellular Autophagy ◽  
Quantitative Results ◽  
Lysosomal System ◽  
Morphologic Data

The morphological evaluation of fractions isolated by a variety of centrifugation methods has, until recently, been a qualitative one, based essentially on subjective impressions of small samples whose representativeness was not known. The lack of quantitative information about components of these fractions severely limited the usefulness of these morphologic data and made correlation with biochemical results rather difficult. In response to this situation, Baudhuin et al., and later Baudhuin and Berthet presented a method which circumvented previous problems and gave quantitative results directly comparable to those obtained by other methods. This method has been used in recent investigations concerned with the role of the lysosomal system in cellular autophagy carried out in this laboratory.

scholarly journals Molecular Insights into the Multifunctional Role of Natural Compounds: Autophagy Modulation and Cancer Prevention

Biomedicines ◽  
2020 ◽  
Vol 8 (11) ◽  
pp. 517
Author(s):  
Md. Ataur Rahman ◽  
MD. Hasanur Rahman ◽  
Md. Shahadat Hossain ◽  
Partha Biswas ◽  
Rokibul Islam ◽  
...  
Keyword(s):  
Side Effects ◽  
Cancer Treatment ◽  
Cancer Prevention ◽  
Stress Responses ◽  
Natural Compounds ◽  
Degradation Pathway ◽  
Synthetic Chemicals ◽  
Cellular Autophagy ◽  
Autophagy Pathway

Autophagy is a vacuolar, lysosomal degradation pathway for injured and damaged protein molecules and organelles in eukaryotic cells, which is controlled by nutrients and stress responses. Dysregulation of cellular autophagy may lead to various diseases such as neurodegenerative disease, obesity, cardiovascular disease, diabetes, and malignancies. Recently, natural compounds have come to attention for being able to modulate the autophagy pathway in cancer prevention, although the prospective role of autophagy in cancer treatment is very complex and not yet clearly elucidated. Numerous synthetic chemicals have been identified that modulate autophagy and are favorable candidates for cancer treatment, but they have adverse side effects. Therefore, different phytochemicals, which include natural compounds and their derivatives, have attracted significant attention for use as autophagy modulators in cancer treatment with minimal side effects. In the current review, we discuss the promising role of natural compounds in modulating the autophagy pathway to control and prevent cancer, and provide possible therapeutic options.

scholarly journals Cellular autophagy in α cells plays a role in the maintenance of islet architecture

2019 ◽  
Author(s):  
Miwa Himuro ◽  
Takeshi Miyatsuka ◽  
Luka Suzuki ◽  
Masaki Miura ◽  
Takehiro Katahira ◽  
...  
Keyword(s):  
Cellular Proliferation ◽  
Cell Function ◽  
Multilayered Structure ◽  
Β Cell ◽  
Cellular Autophagy ◽  
Β Cell Function ◽  
And Function ◽  
And Control ◽  
Deficient Mice

Abstract Autophagy is known to play a pivotal role in intracellular quality control through the degradation of subcellular damaged organelles and components. Whereas autophagy is essential for maintaining β-cell function in pancreatic islets, it remains unclear as to how the cellular autophagy affects the homeostasis and function of glucagon-secreting α cells. To investigate the role of autophagy in α cells, we generated a mutant mouse model lacking Atg7, a key molecule for autophagosome formation, specifically in α cells. Histological analysis demonstrated an increased number of glucagon-positive cells, with a multilayered structure, in the islets under Atg7 deficiency, although metabolic profiles, such as body weight, blood glucose and plasma glucagon levels, were comparable between Atg7-deficient mice and control littermates. Consistent with our previous findings that Atg7 deficiency suppressed β-cell proliferation, cellular proliferation was suppressed in Atg7-deficient α cells. These findings suggest that α-cell autophagy plays a role in maintaining α-cell area and normal islet architecture, but appears to be dispensable for metabolic homeostasis.

scholarly journals Interaction of Poliovirus Capsid Proteins with the Cellular Autophagy Pathway

2021 ◽  
Author(s):  
Anna Zimina ◽  
Ekaterina G. Viktorova ◽  
Seyedemahsa Moghimi ◽  
Jules Nchoutmboube ◽  
George A. Belov
Keyword(s):  
Capsid Proteins ◽  
Replication Proteins ◽  
Cell Type ◽  
Viral Antigens ◽  
Viral Proteases ◽  
Cellular Autophagy ◽  
Infected Cells ◽  
Cell Type Specific ◽  
Autophagy Pathway

The capsid precursor P1 constitutes the N-terminal part of the enterovirus poly-protein. It is processed into VP0, VP3, and VP1 by the viral proteases, and VP0 is cleaved autocatalytically into VP4 and VP2. We observed that poliovirus VP0 is recognized by an antibody against a cellular autophagy protein LC3A. The LC3A-like epitope overlapped the VP4/VP2 cleavage site. Individually expressed VP0-EGFP and P1 strongly colocalized with a marker of selective autophagy p62/SQSTM1. To assess the role of capsid proteins in autophagy development we infected different cells with poliovirus or encapsidated polio replicon coding for only the replication proteins. We analyzed the processing of LC3B and p62/SQSTM1, markers of the initiation and completion of the autophagy pathway, and systematically investigated the association of the viral antigens with these au-tophagy proteins in infected cells. We observed cell-type specific development of autophagy upon infection and found that only the virion signal strongly co-localized with p62/SQSTM1 early in infection. Collectively, our data suggest that activation of autophagy is an antiviral response, and that capsid proteins con-tain determinants targeting them to p62/SQSTM1-dependent sequestration. Such a strategy may control the level of capsid proteins so that viral RNAs are not re-moved from the replication/translation pool prematurely.

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