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/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Although remarkable developments in lung cancer treatments have been made,lung cancer remains the leading cause of cancer mortality worldwide. Epidermalgrowth factor receptor (EGFR) is occasionally mutated in non-small cell lung cancerand heterogeneity in treatment response results from different EGFR mutations.In the present study, we found that centrocyte/centroblast marker 1 (CM1), previouslyreported as a possible apoptosis inducer of B lymphoma cells, is expressed onboth A549 with wild‑type EGFR and HCC827 with mutant EGFR lung cancer cells. Ligationof CM1 with anti-CM1 mAb enhanced apoptosis in both lung cancer cell lines throughgeneration of reactive oxygen species (ROS) and disruption of mitochondrial membranepotential, however, the signaling mechanisms differed from each other. Furtherstudies to investigate the signaling mechanisms identified that ligation of CM1‑inducedapoptosis in A549 cell involved FasL expression, caspase-8, ERK1/2 and Akt kinase,whereas apoptosis of HCC827 cells was induced through caspase-9, JNK and c-jun‑dependentpathways. Taken together, we suggest that CM1 could be developed as a therapeutictarget of lung cancer regardless of EGFR mutation status.

Ligation of CM1 enhances apoptosis of lung cancer cells through different mechanisms in conformity with EGFR mutation