English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Plus

Presents the zaia usage as premium feature

ZAIA

Presents the pdf analysis as premium feature

PDF Analysis

Insights

Presents the summarisation as premium feature

Summarisation

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the access of premium content as premium feature

Premium Content

Zendy Tools

Zendy Open

Cisplatin (cis-diamminedichloroplatinum (II)) is the backbone of negatively regulates cisplatin-induced autophagy and apoptosis [8]. chemotherapy, above all in lung cancers (small and non-small cell lung cancer (SCLC and NSCLC)). The drug was known as Peyrone's salt for more than 100 years until it was recognized as an anti-cancer drug through a serendipitous finding in 1969. Cisplatin has been used in cancer medicine since the 1972 [1], albeit, cisplatin-based chemotherapy still provides short-lived progression-free survival in advanced NSCLC (Fig. 1). Breast cancer susceptibility gene 1 (BRCA1)-customized cisplatin therapy was unsuccessful in two randomized clinical trials in European and Chinese NSCLC patients [2]. The mechanisms of cisplatin resistance have been related to nucleotide excision repair (NER), aswell as other DNA repair pathways that includes BRCA1 modulating stressinduced apoptosis signaling cascade constituting H-ras oncogene, mitogen-activated protein kinase 4, JNK, Fas and Fas ligand, and the activation of caspase-9 [1,3,4]. The intrinsicmitochondrial apoptosis pathway is controlled by interactions between the pro-apoptotic and antiapoptotic members of the BCL2 protein family. One central gene is BCL2L11 (also known as BIM). Tumor cells mostly use the mitogenactivated protein kinase (MAPK) proteasome axis to escape from BCL211 induced apoptosis. The amount of BCL211 expression can control the fate of tumor cells [4]. MAPK pathways modulate cisplatin sensitivity.MAPKs encompass a family of kinases that are divided into three subfamilies: c-Jun N-terminal kinase 1/2 (JNK 1/2), p38 and extracellular-signal-regulated kinase (ERK). The DNA damage response also involves the ATR-Claspin-Chk1 pathway [1,5]. Intriguingly, the endoplasmic reticulum (ER) resident PERK has been shown to regulate ERK phosphorylation and inhibit the ATR-Claspin-Chk1 pathway [6]. Less known is the role of autophagy and its regulation of the response to chemotherapy. Autophagy involves the formation of doublemembrane vesicles, known as autophagosomes for cargo delivery to the lysosomes. Membranes from the ER, the outer membrane of mitochondria, the Golgi apparatus, as well as plasmamembranes contribute to its formation [7]. In the current EBioMedicine article, Bai and colleagues uncover a common mechanism of resistance to cisplatin in NSCLC through the protein disulfide isomerase family-6 (PDIA6), that

Disulfide isomerase family-6 mediates cisplatin resistance by interfering with apoptosis and autophagy