Autophagy in the physiological endometrium and cancer

Devis-Jáuregui, Laura; Eritja, Núria; Davis, Meredith Leigh; Matías‐Guiu, Xavier; Llobet‐Navas, David

doi:10.1080/15548627.2020.1752548

Cited by 139 publications

(95 citation statements)

References 146 publications

(152 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It is commonly considered a cell survival mechanism. Thus, in an attempt to maintain the intracellular balance after chemotherapy, autophagy may represent a further mechanism for cancer cells to escape cell death [10,15,16]. Autophagy has been observed to protect cancer cells from apoptosis upon treatment with some anticancer drugs and it may drive the acquisition of chemoresistance [17][18][19].…”

Section: Autophagymentioning

confidence: 99%

BIRC3 and BIRC5: multi‐faceted inhibitors in cancer

Frazzi

2021

Cell Biosci

126

View full text Add to dashboard Cite

Background The evasion from apoptosis is a common strategy adopted by most tumors, and inhibitors of apoptosis proteins (IAPs) are among the most studied molecular and therapeutic targets. BIRC3 (cellular IAP2) and BIRC5 (survivin) are two of the eight members of the human IAPs family. This family is characterized by the presence of the baculoviral IAP repeat (BIR) domains, involved in protein-protein interactions. In addition to the BIR domains, IAPs also contain other important domains like the C-terminal ubiquitin-conjugating (UBC) domain, the caspase recruitment (CARD) domain and the C-terminal Ring zinc-finger (RING) domain. Main body BIRC3 and BIRC5 have been characterized in some solid and hematological tumors and are therapeutic targets for the family of drugs called “Smac mimetics”. Many evidences point to the pro-survival and antiapoptotic role of BIRC3 in cancer cells, however, not all the data are consistent and the resulting picture is heterogeneous. For instance, BIRC3 genetic inactivation due to deletions or point mutations is consistently associated to shorter progression free survival and poor prognosis in chronic lymphocytic leukemia patients. BIRC3 inactivation has also been associated to chemoimmunotherapy resistance. On the contrary, the progression from low grade gliomas to high grade gliomas is accompanied by BIRC3 expression increase, which bears relevant prognostic consequences. Due to the relationship between BIRC3, MAP3K14 and the non-canonical NF-kB pathway, BIRC3 inactivation bears consequences also on the tumor cells relying on NF-kB pathway to survive. BIRC5, on the contrary, is commonly considered an anti-apoptotic molecule, promoting cell division and tumor progression and it is widely regarded as potential therapeutic target. Conclusions The present manuscript collects and reviews the most recent literature concerning the role played by BIRC3 and BIRC5 in cancer cells, providing useful information for the choice of the best therapeutic targets.

show abstract

Section: Autophagymentioning

confidence: 99%

BIRC3 and BIRC5: multi‐faceted inhibitors in cancer

Frazzi

2021

Cell Biosci

126

View full text Add to dashboard Cite

show abstract

“…HIF1A , known as hypoxia-inducible factor 1α, serves as a regulator of the adaptive response to hypoxia [ 16 , 40 ]. Autophagy induced by hypoxia is a key factor in the progression of various tumors [ 41 , 42 , 43 ]. Although HIF1A activation likely induces the development of aortic dissection, the relationship between autophagy and hypoxia is poorly understood [ 44 , 45 ].…”

Section: Discussionmentioning

confidence: 99%

Exaggerated Autophagy in Stanford Type A Aortic Dissection: A Transcriptome Pilot Analysis of Human Ascending Aortic Tissues

Zhou

Liu

Zhu

et al. 2020

Genes

View full text Add to dashboard Cite

Stanford type A aortic dissection (TAAD) is one of the most dangerous diseases of acute aortic syndrome. Molecular pathological studies on TAAD can aid in understanding the disease comprehensively and can provide insights into new diagnostic markers and potential therapeutic targets. In this study, we defined the molecular pathology of TAAD by performing transcriptome sequencing of human ascending aortic tissues. Pathway analysis revealed that activated inflammation, cell death and smooth muscle cell degeneration are the main pathological changes in aortic dissection. However, autophagy is considered to be one of the most important biological processes, regulating inflammatory reactions and degenerative changes. Therefore, we focused on the pathological role of autophagy in aortic dissection and identified 10 autophagy-regulated hub genes, which are all upregulated in TAAD. These results indicate that exaggerated autophagy participates in the pathological process of aortic dissection and may provide new insight for further basic research on TAAD.

show abstract

“…Autophagy is a tightly regulated and highly conserved lysosomal degradation pathway for the degradation of long-lived proteins and cytoplasmic organelles. Recent accumulating data point to autophagy as a key player in various human diseases, such as cancer [17] .Apoptosis is the process by which a cell ceases to grow and divide, resulting in the controlled death of the cell. The initiation of apoptosis depends on the activation of a series of cysteine-aspartic proteases known as caspases [18].…”

Section: Discussionmentioning

confidence: 99%

WITHDRAWN: Mig-6 Promotes the Apoptosis and Inhibits of the Flux of Autophagy in HCC Cell Lines Through Modulating Mig-6/miR-193a-3p/TGF-β2 Axis

Tian

Hong

et al. 2020

Preprint

View full text Add to dashboard Cite

Abstract Background:Mitogen-inducible gene 6 (Mig-6) is a tumor suppressor gene that plays an important role in many types of cancers by interacting with EGFR. Thus far, little is known about the molecular mechanism of Mig-6 in hepatocellular carcinoma (HCC). Also, the relationship between Mig-6 and miRNAs needs to be elucidated. Therefore, this study first aimed to find whether Mig-6 could promote apoptosis and inhibition of the flux of autophagy by its downstream miRNA in HCC cell lines. Methods: Two cell lines, HepG2and HLE, were used in this study. Mig-6 overexpression and knockdown models , miR-193a mimics and inhibitors models,were established. MiRNA microarray profiling were used to verified Mig-6 regulated- miRNA. Real-time PCR, Western blot analysis were carried out to detect RNA and protein expression.Evaluation of fluorescent LC3 puncta and cell fow cytometer assay were used to test the autophagy and apoptosis respectively. Results: Mig-6 induced the apoptosis and reduced the autophagy of HCC cell lines. MiR-193a-3p is a Mig-6-regulated miRNA in Mig-6 overexpression model, and miR-193a-3p affected the apoptosis and autophagy of HCC cells by regulating the expression of TGF-β2. Additionally, the relationship between Mig-6 and transforming growth factor TGF-β2 was explored in depth for the first time.Conclusion:These findings revealed an important regulatory axis Mig-6/miR-193a-3p/TGF-β2 in the apoptosis and autophagy of HCC cells, providing a novel insight into the therapeutic target in HCC.

show abstract

Autophagy in the physiological endometrium and cancer

Cited by 139 publications

References 146 publications

BIRC3 and BIRC5: multi‐faceted inhibitors in cancer

BIRC3 and BIRC5: multi‐faceted inhibitors in cancer

Exaggerated Autophagy in Stanford Type A Aortic Dissection: A Transcriptome Pilot Analysis of Human Ascending Aortic Tissues

WITHDRAWN: Mig-6 Promotes the Apoptosis and Inhibits of the Flux of Autophagy in HCC Cell Lines Through Modulating Mig-6/miR-193a-3p/TGF-β2 Axis

Contact Info

Product

Resources

About