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Expression of Derlin-1 and its effect on expression of autophagy marker genes under endoplasmic reticulum stress in lung cancer cells.

Xu L, Wang ZH, Xu D, Lin G, Li DR, Wan T, Guo SL - Cancer Cell Int. (2014)

Bottom Line: Knockdown of Derlin-1 did not affect Beclin 1 and LC3II expression but disrupted the degradation of p62 under ER stress, which resulted in the blockage of autophagy flux.Furthermore, Derlin-1 and p62 were observed to interact under ER stress.Derlin-1 may function in tumour progression partially by interacting with p62.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Respiratory Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.

ABSTRACT

Background: Recent findings indicated that Derlin-1 has an important function in tumour progression. In this study, we aimed to determine whether Derlin-1 has an oncogene function as a cross-talk molecule with autophagy.

Methods: Cancer cells were treated with tunicamycin (TM) for 8 and 24 h. The expression of Derlin-1 and autophagy-related genes was determined by western blot. Autophagy was analysed by fluorescence microscopy after staining the cancer cells with monodansylcadaverine. The interaction between Derlin-1 and other proteins was identified using co-immunoprecipitation assay.

Results: Our study demonstrated high Derlin-1 expression levels in most non-small lung cancer cell lines. Derlin-1 expression was enhanced under endoplasmic reticulum (ER) stress. Previous studies revealed that TM triggers the initiation of autophagy by activating Beclin 1, converting LC3I to LC3II and degrading p62. Knockdown of Derlin-1 did not affect Beclin 1 and LC3II expression but disrupted the degradation of p62 under ER stress, which resulted in the blockage of autophagy flux. Furthermore, Derlin-1 and p62 were observed to interact under ER stress.

Conclusion: This study is the first report about the interaction between Derlin-1 and p62. Derlin-1 may function in tumour progression partially by interacting with p62.

No MeSH data available.


Related in: MedlinePlus

Detection of Derlin-1 expression in NCI-N446 cells after TM treatment using western blot. GRP78 expression was induced by ER stress. Expression of Derlin-1, autophagy gene Beclin 1 and LC3II increased under ER stress, but p62 expression decreased, indicating the induction of autophagy.
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Figure 2: Detection of Derlin-1 expression in NCI-N446 cells after TM treatment using western blot. GRP78 expression was induced by ER stress. Expression of Derlin-1, autophagy gene Beclin 1 and LC3II increased under ER stress, but p62 expression decreased, indicating the induction of autophagy.

Mentions: We detected Derlin-1 expression in NCI-H446 cells using ER stress-inducing agent TM. NCI-H446 cells were used because of their low endogenous level of Derlin-1. ER stress can be evoked by TM within a short time, so we detected gene expression 8 and 24 h after TM exposure. As an ER chaperone, glucose-regulated protein 78 (GRP78) is commonly used as a marker of ER stress. Increased GRP78 expression indicated that ER stress was triggered by TM treatment. Derlin-1 expression significantly increased after 8 and 24 h of TM treatment (Figure 2). In A549 cells with high endogenous levels of Derlin-1, Derlin-1 expression only slightly increased by TM treatment.


Expression of Derlin-1 and its effect on expression of autophagy marker genes under endoplasmic reticulum stress in lung cancer cells.

Xu L, Wang ZH, Xu D, Lin G, Li DR, Wan T, Guo SL - Cancer Cell Int. (2014)

Detection of Derlin-1 expression in NCI-N446 cells after TM treatment using western blot. GRP78 expression was induced by ER stress. Expression of Derlin-1, autophagy gene Beclin 1 and LC3II increased under ER stress, but p62 expression decreased, indicating the induction of autophagy.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4061450&req=5

Figure 2: Detection of Derlin-1 expression in NCI-N446 cells after TM treatment using western blot. GRP78 expression was induced by ER stress. Expression of Derlin-1, autophagy gene Beclin 1 and LC3II increased under ER stress, but p62 expression decreased, indicating the induction of autophagy.
Mentions: We detected Derlin-1 expression in NCI-H446 cells using ER stress-inducing agent TM. NCI-H446 cells were used because of their low endogenous level of Derlin-1. ER stress can be evoked by TM within a short time, so we detected gene expression 8 and 24 h after TM exposure. As an ER chaperone, glucose-regulated protein 78 (GRP78) is commonly used as a marker of ER stress. Increased GRP78 expression indicated that ER stress was triggered by TM treatment. Derlin-1 expression significantly increased after 8 and 24 h of TM treatment (Figure 2). In A549 cells with high endogenous levels of Derlin-1, Derlin-1 expression only slightly increased by TM treatment.

Bottom Line: Knockdown of Derlin-1 did not affect Beclin 1 and LC3II expression but disrupted the degradation of p62 under ER stress, which resulted in the blockage of autophagy flux.Furthermore, Derlin-1 and p62 were observed to interact under ER stress.Derlin-1 may function in tumour progression partially by interacting with p62.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Respiratory Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.

ABSTRACT

Background: Recent findings indicated that Derlin-1 has an important function in tumour progression. In this study, we aimed to determine whether Derlin-1 has an oncogene function as a cross-talk molecule with autophagy.

Methods: Cancer cells were treated with tunicamycin (TM) for 8 and 24 h. The expression of Derlin-1 and autophagy-related genes was determined by western blot. Autophagy was analysed by fluorescence microscopy after staining the cancer cells with monodansylcadaverine. The interaction between Derlin-1 and other proteins was identified using co-immunoprecipitation assay.

Results: Our study demonstrated high Derlin-1 expression levels in most non-small lung cancer cell lines. Derlin-1 expression was enhanced under endoplasmic reticulum (ER) stress. Previous studies revealed that TM triggers the initiation of autophagy by activating Beclin 1, converting LC3I to LC3II and degrading p62. Knockdown of Derlin-1 did not affect Beclin 1 and LC3II expression but disrupted the degradation of p62 under ER stress, which resulted in the blockage of autophagy flux. Furthermore, Derlin-1 and p62 were observed to interact under ER stress.

Conclusion: This study is the first report about the interaction between Derlin-1 and p62. Derlin-1 may function in tumour progression partially by interacting with p62.

No MeSH data available.


Related in: MedlinePlus