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Article ; Online: Autophagy genes as tumor suppressors.

Liang, Chengyu / Jung, Jae U

2009 Volume 22, Issue 2, Page(s) 226–233

Abstract: ... basis of autophagy genes and their biological outputs during tumor development. A better understanding ... of the mechanistic link between cellular autophagy and tumor growth control may ultimately better human cancer ... Autophagy, originally described as a universal lysosome-dependent bulk degradation of cytoplasmic ...

Abstract	Autophagy, originally described as a universal lysosome-dependent bulk degradation of cytoplasmic components upon nutrient deprivation, has since been shown to influence diverse aspects of homeostasis and is implicated in a wide variety of pathological conditions, including cancer. The list of autophagy-related (Atg) genes associated with the initiation and progression of human cancer as well as with responses to cancer therapy continues to grow as these genes are being discovered. However, whether Atg genes work through their expected mechanisms of autophagy regulation and/or through as-yet-undefined functions in the development of cancer remains to be further clarified. Here we review recent advances in the knowledge of the molecular basis of autophagy genes and their biological outputs during tumor development. A better understanding of the mechanistic link between cellular autophagy and tumor growth control may ultimately better human cancer treatments.
MeSH term(s)	Animals ; Autophagy/genetics ; Genes, Tumor Suppressor ; Humans ; Neoplasms/genetics ; Neoplasms/pathology
Language	English
Publishing date	2009-11-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1026381-0
ISSN	1879-0410 ; 0955-0674
ISSN (online)	1879-0410
ISSN	0955-0674
DOI	10.1016/j.ceb.2009.11.003
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Article: The role of chaperone-mediated autophagy in drug resistance.

Teixeira, Ana Beatriz da Silva / Ramalho, Maria Carolina Clares / Souza, Izadora de / Andrade, Izabela Amélia Marques de / Osawa, Isabeli Yumi Araújo / Guedes, Camila Banca / Oliveira, Beatriz Silva de / Souza Filho, Cláudio Henrique Dahne de / Silva, Tainá Lins da / Moreno, Natália Cestari / Latancia, Marcela Teatin / Rocha, Clarissa Ribeiro Reily

Genetics and molecular biology

2024 Volume 47, Issue Suppl 1, Page(s) e20230317

Abstract: ... the degradation of proteins by CMA can offer important advantages for tumorigenesis, since tumor suppressor proteins are CMA ... into CMA's contribution to tumor progression has accelerated rapidly. Therefore, we now understand ... in cancer treatment, the modulation of autophagy has emerged as a promising alternative that has achieved ...

Abstract	In the search for alternatives to overcome the challenge imposed by drug resistance development in cancer treatment, the modulation of autophagy has emerged as a promising alternative that has achieved good results in clinical trials. Nevertheless, most of these studies have overlooked a novel and selective type of autophagy: chaperone-mediated autophagy (CMA). Following its discovery, research into CMA's contribution to tumor progression has accelerated rapidly. Therefore, we now understand that stress conditions are the primary signal responsible for modulating CMA in cancer cells. In turn, the degradation of proteins by CMA can offer important advantages for tumorigenesis, since tumor suppressor proteins are CMA targets. Such mutual interaction between the tumor microenvironment and CMA also plays a crucial part in establishing therapy resistance, making this discussion the focus of the present review. Thus, we highlight how suppression of LAMP2A can enhance the sensitivity of cancer cells to several drugs, just as downregulation of CMA activity can lead to resistance in certain cases. Given this panorama, it is important to identify selective modulators of CMA to enhance the therapeutic response.
Language	English
Publishing date	2024-05-31
Publishing country	Brazil
Document type	Journal Article
ZDB-ID	1445712-x
ISSN	1678-4685 ; 1415-4757
ISSN (online)	1678-4685
ISSN	1415-4757
DOI	10.1590/1678-4685-GMB-2023-0317
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Zs.A 3079: Show issues

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Article ; Online: Microorganism-regulated autophagy in gastrointestinal cancer.

Xu, Jun-Yu / Fan, Jiao-Xiu / Hu, Min / Zeng, Jun

PeerJ

2023 Volume 11, Page(s) e16130

Abstract: ... in tumors as both tumor suppressor and tumor promoter. Many studies have shown that autophagy plays ... in the microbial community during tumorigenesis. Autophagy is an important intracellular homeostatic process ... where defective proteins and organelles are degraded and recycled under stress. Autophagy plays a dual role ...

Abstract	Gastrointestinal cancer has always been one of the most urgent problems to be solved, and it has become a major global health issue. Microorganisms in the gastrointestinal tract regulate normal physiological and pathological processes. Accumulating evidence reveals the role of the imbalance in the microbial community during tumorigenesis. Autophagy is an important intracellular homeostatic process, where defective proteins and organelles are degraded and recycled under stress. Autophagy plays a dual role in tumors as both tumor suppressor and tumor promoter. Many studies have shown that autophagy plays an important role in response to microbial infection. Here, we provide an overview on the regulation of the autophagy signaling pathway by microorganisms in gastrointestinal cancer.
MeSH term(s)	Humans ; Autophagy/genetics ; Gastrointestinal Neoplasms/genetics ; Genes, Tumor Suppressor ; Carcinogenesis ; Cell Transformation, Neoplastic
Language	English
Publishing date	2023-09-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2703241-3
ISSN	2167-8359 ; 2167-8359
ISSN (online)	2167-8359
ISSN	2167-8359
DOI	10.7717/peerj.16130
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Article ; Online: Degradative autophagy regulates the homeostasis of miRnas to control cancer development.

Wu, Shan-Ying / Chu, Chien-An / Lan, Sheng-Hui / Liu, Hsiao-Sheng

Autophagy

2024 , Page(s) 1–3

Abstract: Macroautophagy/autophagy acts as an anti-tumor mechanism in early cancer stages but promotes growth ... in established tumors. Similarly, miRNAs function as tumor suppressors or oncogenes, depending on their target ... genes. This reciprocal relationship between autophagy and miRNAs is a well-studied area, primarily ...

Abstract	Macroautophagy/autophagy acts as an anti-tumor mechanism in early cancer stages but promotes growth in established tumors. Similarly, miRNAs function as tumor suppressors or oncogenes, depending on their target genes. This reciprocal relationship between autophagy and miRNAs is a well-studied area, primarily focused on how miRNAs regulate autophagy-related genes. Our research provides innovative insights into how autophagy selectively controls miRNAs. For instance,
Language	English
Publishing date	2024-03-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2024.2312035
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Zs.A 6741: Show issues

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Article ; Online: VHL suppresses autophagy and tumor growth through PHD1-dependent Beclin1 hydroxylation.

Wang, Zheng / Yan, Meisi / Ye, Leiguang / Zhou, Qimin / Duan, Yuran / Jiang, Hongfei / Wang, Lei / Ouyang, Yuan / Zhang, Huahe / Shen, Yuli / Ji, Guimei / Chen, Xiaohan / Tian, Qi / Xiao, Liwei / Wu, Qingang / Meng, Ying / Liu, Guijun / Ma, Leina / Lei, Bo /

Lu, Zhimin / Xu, Daqian

The EMBO journal

2024 Volume 43, Issue 6, Page(s) 931–955

Abstract: ... abrogates VHL-mediated autophagy inhibition and significantly reduces the tumor-suppressing effect of VHL ... mouse tumors with autophagy inhibitors and HIF2α inhibitors suppresses tumor growth. These findings ... However, whether VHL possesses HIF-independent tumor-suppressing activity remains largely unclear. Here, we demonstrate ...

Abstract	The Von Hippel-Lindau (VHL) protein, which is frequently mutated in clear-cell renal cell carcinoma (ccRCC), is a master regulator of hypoxia-inducible factor (HIF) that is involved in oxidative stresses. However, whether VHL possesses HIF-independent tumor-suppressing activity remains largely unclear. Here, we demonstrate that VHL suppresses nutrient stress-induced autophagy, and its deficiency in sporadic ccRCC specimens is linked to substantially elevated levels of autophagy and correlates with poorer patient prognosis. Mechanistically, VHL directly binds to the autophagy regulator Beclin1, after its PHD1-mediated hydroxylation on Pro54. This binding inhibits the association of Beclin1-VPS34 complexes with ATG14L, thereby inhibiting autophagy initiation in response to nutrient deficiency. Expression of non-hydroxylatable Beclin1 P54A abrogates VHL-mediated autophagy inhibition and significantly reduces the tumor-suppressing effect of VHL. In addition, Beclin1 P54-OH levels are inversely correlated with autophagy levels in wild-type VHL-expressing human ccRCC specimens, and with poor patient prognosis. Furthermore, combined treatment of VHL-deficient mouse tumors with autophagy inhibitors and HIF2α inhibitors suppresses tumor growth. These findings reveal an unexpected mechanism by which VHL suppresses tumor growth, and suggest a potential treatment for ccRCC through combined inhibition of both autophagy and HIF2α.
MeSH term(s)	Animals ; Humans ; Mice ; Autophagy ; Beclin-1/genetics ; Beclin-1/metabolism ; Carcinoma, Renal Cell/metabolism ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Hydroxylation ; Kidney Neoplasms/metabolism ; Procollagen-Proline Dioxygenase/metabolism ; Von Hippel-Lindau Tumor Suppressor Protein/genetics ; Von Hippel-Lindau Tumor Suppressor Protein/metabolism
Chemical Substances	Beclin-1 ; PHD1 protein, mouse (EC 1.14.11.2) ; Procollagen-Proline Dioxygenase (EC 1.14.11.2) ; VHL protein, human (EC 6.3.2.-) ; Von Hippel-Lindau Tumor Suppressor Protein (EC 2.3.2.27) ; EGLN2 protein, human (EC 1.14.11.29) ; BECN1 protein, human
Language	English
Publishing date	2024-02-15
Publishing country	England
Document type	Journal Article
ZDB-ID	586044-1
ISSN	1460-2075 ; 0261-4189
ISSN (online)	1460-2075
ISSN	0261-4189
DOI	10.1038/s44318-024-00051-2
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Zs.A 1808: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Autophagy Plays a Crucial Role in Ameloblast Differentiation.

Iwaya, C / Suzuki, A / Shim, J / Ambrose, C G / Iwata, J

Journal of dental research

2023 Volume 102, Issue 9, Page(s) 1047–1057

Abstract: ... in the enamel, a condition known as amelogenesis imperfecta. Here, we report that mice with deficient autophagy ... Tooth enamel is generated by ameloblasts. Any failure in amelogenesis results in defects ...

Abstract	Tooth enamel is generated by ameloblasts. Any failure in amelogenesis results in defects in the enamel, a condition known as amelogenesis imperfecta. Here, we report that mice with deficient autophagy in epithelial-derived tissues (
MeSH term(s)	Mice ; Animals ; Ameloblasts/metabolism ; Amelogenesis Imperfecta/genetics ; X-Ray Microtomography ; NF-E2-Related Factor 2/metabolism ; Amelogenesis/genetics ; Mice, Knockout ; Tumor Suppressor Proteins/metabolism ; Repressor Proteins/metabolism
Chemical Substances	NF-E2-Related Factor 2 ; Tumor Suppressor Proteins ; Bcl11b protein, mouse ; Repressor Proteins
Language	English
Publishing date	2023-05-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	80207-4
ISSN	1544-0591 ; 0022-0345
ISSN (online)	1544-0591
ISSN	0022-0345
DOI	10.1177/00220345231169220
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Ul III Zs.75: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MO 262: Show issues

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Article ; Online: Amonafide Induces HUVEC Senescence by Inhibiting Autophagy.

Xia, Jing / Zhou, Yu / He, Siyue / Vashisth, Manoj Kumar / Jia, Huijie / Dai, Qianlong / He, Yufen / Wang, Xiaobo

Discovery medicine

2023 Volume 35, Issue 176, Page(s) 264–274

Abstract: ... cellular senescence in our experiments. Amonafide-induced cellular aging by inhibiting autophagy and activating ... The experiments of expression of genes and proteins associated with aging were carried out with HUVEC cell lines ...

Abstract	Background: Amonafide (Amo), due to hematotoxicity and digestive tract symptoms, the clinical application of which is limited. Several studies have reported that chemotherapy side effects are closely related to cellular senescence accumulation. Our study aims to examine whether amonafide causes senescence in human umbilical vein endothelial cell (HUVEC) lines and investigate its mechanisms associated with senescence. Methods: The experiments of expression of genes and proteins associated with aging were carried out with HUVEC cell lines. The experiments were divided into a control group and an amonafide group with different days. The HUVEC senescence cells were detected by SA-β-Gal staining, Western blotting detected the protein levels of p16, p53, AMPK (Adenosine 5'-Monophosphate (AMP)-Activated Protein Kinase), mTOR (mechanistic Target of Rapamycin), p62, and LC3 (microtubule-associated protein1 light chain 3, MAP1LC3). Fluorescence detected the expression of mRFP (monomeric Red Fluorescent Protein)-GFP (Green Fluorescent Protein)-LC3 and LC3 puncta of HUVEC cells. RT-qPCR (Real-Time Quantitative Polymerase Chain Reaction) tested the expressions of Results: Here, we reported that amonafide resulted in an increased proportion of SA-β-Gal positive cells, high expression of aging-related proteins (p53 Conclusions: We first discovered that amonafide caused normal cellular senescence in our experiments. Amonafide-induced cellular aging by inhibiting autophagy and activating the mTOR pathway. The findings may offer new strategies for managing adverse reactions to amonafide.
MeSH term(s)	Humans ; Human Umbilical Vein Endothelial Cells/chemistry ; Human Umbilical Vein Endothelial Cells/metabolism ; Interleukin-8/metabolism ; Interleukin-8/pharmacology ; Tumor Suppressor Protein p53/analysis ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Interleukin-6/metabolism ; TOR Serine-Threonine Kinases/metabolism ; Autophagy ; Cellular Senescence/physiology
Chemical Substances	amonafide (1Q8D39N37L) ; Interleukin-8 ; Tumor Suppressor Protein p53 ; Interleukin-6 ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2023-06-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2415544-5
ISSN	1944-7930 ; 1944-7930
ISSN (online)	1944-7930
ISSN	1944-7930
DOI	10.24976/Discov.Med.202335176.27
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Article ; Online: Delineating the twin role of autophagy in lung cancer.

Zhang, Shaoqin / Qian, Ye / Ye, Luhai

Biologia futura

2023 Volume 74, Issue 1-2, Page(s) 119–135

Abstract: ... stages, autophagy has been shown to act as a tumor-promoting system as it may help the cancer cells ... we discuss the various aspects of autophagy during tumor development, from early to late stages of tumor ... growth. Both the protective role of autophagy in preventing tumor growth and the underlying mechanisms ...

Abstract	Autophagy represents an intracellular defense mechanism equipped within each eukaryotic cells to enable them to cope with variety of physical, chemical, and biological stresses. This mechanism helps to restore the homeostasis and preserve the cellular integrity and function of the cells. In these conditions, such as hypoxia, nutrient deprivation, inhibition of protein synthesis or microbial attack, the process of autophagy is upregulated to maintain cellular homeostasis. The role of autophagy in cancer is an intriguing topic which needs further exploration. This process of autophagy has been many times referred as a double-edged sword in the process of tumorigenesis. In the initial stages, it may act as a tumor suppressor and enable to quench the damaged organelles and harmful molecules generated. In more advanced stages, autophagy has been shown to act as a tumor-promoting system as it may help the cancer cells to cope better with stressful microenvironments. Besides this, autophagy has been associated with development of resistance to anticancer drugs as well as promoting the immune evasion in cancer cells, representing a serious obstacle in cancer treatment and its outcome. Also, autophagy is associated with hallmarks of cancer that may lead to activation of invasion and metastasis. The information on this twin role needs further exploration and deeper understanding of the pathways involved. In this review, we discuss the various aspects of autophagy during tumor development, from early to late stages of tumor growth. Both the protective role of autophagy in preventing tumor growth and the underlying mechanisms adopted with evidence from past studies have been detailed. Further, the role of autophagy in conferring resistance to distinct lung cancer treatment and immune shielding properties has also been discussed. This is essential for further improving on treatment outcome and success rates.
MeSH term(s)	Humans ; Lung Neoplasms ; Autophagy/physiology ; Tumor Microenvironment
Language	English
Publishing date	2023-04-30
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2987596-1
ISSN	2676-8607 ; 2676-8615
ISSN (online)	2676-8607
ISSN	2676-8615
DOI	10.1007/s42977-023-00165-4
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Article ; Online: An Update on Nucleolar Stress: The Transcriptional Control of Autophagy.

Pfister, Astrid S

Cells

2023 Volume 12, Issue 16

Abstract: ... for autophagy-dependent drug resistance of chemotherapy-exposed tumor cells. Given the relatively young age ... can activate autophagy and diverse signaling cascades that might allow initial pro-survival mechanisms ... Nevertheless, it depends on the situation whether the cells undergo autophagy-mediated apoptosis or survive, as seen ...

Abstract	Nucleolar stress reflects a misfunction of the nucleolus caused by a failure in ribosome biogenesis and defective nucleolar architecture. Various causes have been reported, most commonly mutation of ribosomal proteins and ribosome processing factors, as well as interference with these processes by intracellular or ectopic stress, such as RNA polymerase I inhibition, ROS, UV and others. The nucleolus represents the place for ribosome biogenesis and serves as a crucial hub in the cellular stress response. It has been shown to stimulate multiple downstream consequences, interfering with cell growth and survival. Nucleolar stress induction is most classically known to stimulate p53-dependent cell cycle arrest and apoptosis. Nucleolar stress represents a friend and enemy at the same time: From a pathophysiological perspective, inactivation of the nucleolar function by mutation or stress conditions is connected to multiple diseases, such as neurodegeneration, cancer and ribosomopathy syndromes. However, triggering the nucleolar stress response via specific chemotherapeutics, which interfere with nucleolar function, has beneficial effects for anti-cancer therapy. Interestingly, since the nucleolar stress response also triggers p53-independent mechanisms, it possesses the potential to specifically target p53-mutated tumors, which reflects the most common aberration in human cancer. More recent data have shown that the nucleolar stress response can activate autophagy and diverse signaling cascades that might allow initial pro-survival mechanisms. Nevertheless, it depends on the situation whether the cells undergo autophagy-mediated apoptosis or survive, as seen for autophagy-dependent drug resistance of chemotherapy-exposed tumor cells. Given the relatively young age of the research field, precise mechanisms that underly the involvement of autophagy in nucleolar stress are still under investigation. This review gives an update on the emerging contribution of nucleolar stress in the regulation of autophagy at a transcriptional level. It also appears that in autophagy p53-dependent as well as -independent responses are induced. Those could be exploited in future therapies against diseases connected to nucleolar stress.
MeSH term(s)	Humans ; Tumor Suppressor Protein p53/genetics ; Cell Nucleolus ; Autophagy/genetics ; Gene Expression Regulation ; Autophagic Cell Death
Chemical Substances	Tumor Suppressor Protein p53
Language	English
Publishing date	2023-08-15
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12162071
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Article ; Online: Autophagy Paradox: Strategizing Treatment Modality in Melanoma.

Pangilinan, Christian / Xu, Xiaowei / Herlyn, Meenhard / Liang, Chengyu

Current treatment options in oncology

2023 Volume 24, Issue 2, Page(s) 130–145

Abstract: ... In many cases, it is accepted that autophagy operates as a key tumor suppressor mechanism that protects cells ... autonomous autophagy in reshaping tumor microenvironment and maintaining lineage integrity and immune ... leading to the prevailing view that the pro-survival aspect of autophagy might be hijacked by some tumors ...

Abstract	Opinion statement: The primordial autophagy process, originally identified as a starvation response in baker's yeast, has since been shown to have a wide spectrum of functions other than survival. In many cases, it is accepted that autophagy operates as a key tumor suppressor mechanism that protects cells from adverse environmental cues by enforcing homeostasis and maintaining the functional and structural integrity of organelles. Paradoxically, heightened states of autophagy are also seen in some cancers, leading to the prevailing view that the pro-survival aspect of autophagy might be hijacked by some tumors to promote their fitness and pathogenesis. Notably, recent studies have revealed a broad range of cell-autonomous autophagy in reshaping tumor microenvironment and maintaining lineage integrity and immune homeostasis, calling for a renewed understanding of autophagy beyond its classical roles in cell survival. Here, we evaluate the increasing body of literature that argues the "double-edged" consequences of autophagy manipulation in cancer therapy, with a particular focus on highly plastic and mutagenic melanoma. We also discuss the caveats that must be considered when evaluating whether autophagy blockade is the effector mechanism of some anti-cancer therapy particularly associated with lysosomotropic agents. If autophagy proteins are to be properly exploited as targets for anticancer drugs, their diverse and complex roles should also be considered.
MeSH term(s)	Humans ; Neoplasms/therapy ; Melanoma/therapy ; Melanoma/drug therapy ; Autophagy/physiology ; Antineoplastic Agents/therapeutic use ; Cell Survival ; Tumor Microenvironment
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2023-01-21
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	2057351-0
ISSN	1534-6277 ; 1527-2729
ISSN (online)	1534-6277
ISSN	1527-2729
DOI	10.1007/s11864-023-01053-8
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