2022
DOI: 10.3390/cells11233773
|View full text |Cite
|
Sign up to set email alerts
|

Canonical and Noncanonical ER Stress-Mediated Autophagy Is a Bite the Bullet in View of Cancer Therapy

Abstract: Cancer cells adapt multiple mechanisms to counter intense stress on their way to growth. Tumor microenvironment stress leads to canonical and noncanonical endoplasmic stress (ER) responses, which mediate autophagy and are engaged during proteotoxic challenges to clear unfolded or misfolded proteins and damaged organelles to mitigate stress. In these conditions, autophagy functions as a cytoprotective mechanism in which malignant tumor cells reuse degraded materials to generate energy under adverse growing cond… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2

Citation Types

0
2
0

Year Published

2023
2023
2024
2024

Publication Types

Select...
5

Relationship

0
5

Authors

Journals

citations
Cited by 6 publications
(2 citation statements)
references
References 243 publications
0
2
0
Order By: Relevance
“…Therefore, many attempts have been made to achieve anti-cancer effects by inhibiting autophagy while stimulating ER stress. In addition, since autophagy-related genes are difficult to regulate, new anticancer approaches targeting the UPR or non-canonical ER stress are emerging by targeting known upstream signals of autophagy (Alam et al 2022 ).
Figure 4.
…”
Section: Discussionmentioning
confidence: 99%
“…Therefore, many attempts have been made to achieve anti-cancer effects by inhibiting autophagy while stimulating ER stress. In addition, since autophagy-related genes are difficult to regulate, new anticancer approaches targeting the UPR or non-canonical ER stress are emerging by targeting known upstream signals of autophagy (Alam et al 2022 ).
Figure 4.
…”
Section: Discussionmentioning
confidence: 99%
“…Both PIs and histone deacetylation inhibitors have been shown to take advantage of ER stress in myeloma cells [71]. However, higher levels of UPR have also been associated with more malignant and drug-resistant cancers [72,73]. This phenotype may be attributed to the pro-survival functions of GRP78 and the UPR, which would help cancer cells cope with the stressful tumor microenvironment [74].…”
Section: Discussionmentioning
confidence: 99%