PLAC8 promotes adriamycin resistance via blocking autophagy in breast cancer

Chen, Yongxia; Jia, Yunlu; Mao, Misha; Gu, Yi-Jie; Xu, Chenchao; Yang, Jingjing; Hu, Wenxian; Shen, Jun; Hu, Dongyan; Chen, Cong; Li, Zhaoqing; Cao, Feng; Ruan, Jian; Shen, Peng; Zhou, Jichun; Wang, Qun; Wang, Linbo

doi:10.1111/jcmm.16706

Cited by 15 publications

(9 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Reports of PLAC8 cellular localization vary depending on cell type, from cytosolic, to lysosomal ( 23 , 24 ), to the apical domain of differentiated human intestinal epithelium ( 25 ) and/or the inner leaflet of the plasma membrane ( 24 ), although cell surface localization has not been demonstrated. PLAC8 is reported to be involved in multiple complex cellular pathways, including autophagy ( 24 – 27 ), epithelial-mesenchymal transition (EMT), cell motility, innate immune functions ( 22 , 28 ), mitochondrial metabolism, and DNA repair ( 29 ). In particular, autophagy is known to be important in CoV infections.…”

Section: Resultsmentioning

confidence: 99%

Genomewide CRISPR knockout screen identified PLAC8 as an essential factor for SADS-CoVs infection

Tse

Meganck

Araba

et al. 2022

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Significance A potential outbreak of swine acute diarrhea syndrome coronavirus (SADS-CoV) in the human population could be devastating. Using genomewide CRISPR knockout screening, we identified the placenta-associated 8 protein (PLAC8) as an essential host factor for SADS-CoV infection, uncovering a novel antiviral target for CoV infection. The PLAC8-related pathway may also have implications for other CoV infections. Given the ability of SADS-CoV to infect human primary cultures without adaptation, our findings lay the foundation for pandemic preparedness for the potential emergence of SADS-CoVs in response to the One Health Initiative.

show abstract

Section: Resultsmentioning

confidence: 99%

Genomewide CRISPR knockout screen identified PLAC8 as an essential factor for SADS-CoVs infection

Tse

Meganck

Araba

et al. 2022

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…Chemotherapy can inhibit autophagy by regulating microRNA mediated downstream signaling pathways, and promote tumor resistance, such as microRNA-199a-5p 51 and miR-519a. 52 Similar phenomenon was also observed in resistance to cisplatin, 5-fluorouracil and doxorubicin, by activating PI3K-Akt-mTOR signaling to inhibit autophagy, [53][54][55] suggesting that inhibition of autophagy is a key factor.…”

Section: Autophagy Inhibition Promotes Conventional Treatment Resistancementioning

confidence: 57%

Nanoplatform-Mediated Autophagy Regulation and Combined Anti-Tumor Therapy for Resistant Tumors

Yang,

Ding,

Mao

et al. 2024

IJN

View full text Add to dashboard Cite

The overall cancer incidence and death toll have been increasing worldwide. However, the conventional therapies have some obvious limitations, such as non-specific targeting, systemic toxic effects, especially the multidrug resistance (MDR) of tumors, in which, autophagy plays a vital role. Therefore, there is an urgent need for new treatments to reduce adverse reactions, improve the treatment efficacy and expand their therapeutic indications more effectively and accurately. Combination therapy based on autophagy regulators is a very feasible and important method to overcome tumor resistance and sensitize anti-tumor drugs. However, the less improved efficacy, more systemic toxicity and other problems limit its clinical application. Nanotechnology provides a good way to overcome this limitation. Co-delivery of autophagy regulators combined with anti-tumor drugs through nanoplatforms provides a good therapeutic strategy for the treatment of tumors, especially drug-resistant tumors. Notably, the nanomaterials with autophagy regulatory properties have broad therapeutic prospects as carrier platforms, especially in adjuvant therapy. However, further research is still necessary to overcome the difficulties such as the safety, biocompatibility, and side effects of nanomedicine. In addition, clinical research is also indispensable to confirm its application in tumor treatment.

show abstract

“…Our previous research suggested that PLAC8 can promote breast cancer cell growth and participate in the process of tamoxifen and adriamycin resistance. [8][9][10] As we mentioned in our review, 11 PLAC8 also plays an important role in various cancers and is involved in tumor progression, including in programmed cell death,…”

Section: Introductionmentioning

confidence: 90%

Modification of PLAC8 by UFM1 affects tumorous proliferation and immune response by impacting PD-L1 levels in triple-negative breast cancer

Mao

Chen

Yang

et al. 2022

J Immunother Cancer

Self Cite

View full text Add to dashboard Cite

BackgroundTriple-negative breast cancer is characterized by a poor prognosis and lack of targeted treatments, and thus, new targeting markers and therapeutic strategies are urgently needed. We previously indicated that PLAC8 promotes tumorigenesis and exerts multidrug resistance in breast cancer. Therefore, we aimed to characterize the PLAC8-regulated network in triple-negative breast cancer.MethodsWe measured the levels of PLAC8 in breast cancer cell lines and found that PLAC8 is post-translationally modified by ubiquitin-fold modifier 1 (UFM1). Then, we revealed a new regulatory system of PD-L1 by PLAC8 in triple-negative breast cancer. We also tested the molecular functions of PLAC8 in triple-negative breast cancer cell lines and measured the expression of PLAC8 and PD-L1 in breast cancer tissues.ResultsPLAC8 was generally highly expressed in triple-negative breast cancer and could be modified by UFM1, which maintains PLAC8 protein stability. Moreover, PLAC8 could promote cancer cell proliferation and affect the immune response by regulating the level of PD-L1 ubiquitination. Additionally, among patients with breast cancer, the expression of PLAC8 was higher in triple-negative breast cancer than in non-triple-negative breast cancer and positively correlated with the level of PD-L1.ConclusionsOur current study discoveries a new PLAC8-regulated network in triple-negative breast cancer and provides corresponding guidance for the clinical diagnosis and immunotherapy of triple-negative breast cancer.

show abstract

PLAC8 promotes adriamycin resistance via blocking autophagy in breast cancer

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 15 publications

References 27 publications

Genomewide CRISPR knockout screen identified PLAC8 as an essential factor for SADS-CoVs infection

Genomewide CRISPR knockout screen identified PLAC8 as an essential factor for SADS-CoVs infection

Nanoplatform-Mediated Autophagy Regulation and Combined Anti-Tumor Therapy for Resistant Tumors

Modification of PLAC8 by UFM1 affects tumorous proliferation and immune response by impacting PD-L1 levels in triple-negative breast cancer

Contact Info

Product

Resources

About