# Cyclin L1 participates in Adriamycin resistance and progression of osteosarcoma via PI3K/AKT-mTOR pathway

## TL;DR

This study shows that Cyclin L1 contributes to Adriamycin resistance and cancer progression in osteosarcoma through the PI3K/AKT-mTOR pathway.

## Contribution

The study identifies a novel role of Cyclin L1 in Adriamycin resistance and tumor progression in osteosarcoma.

## Key findings

- Cyclin L1 expression is linked to poor prognosis and promotes osteosarcoma cell proliferation and migration.
- Cyclin L1 increases in Adriamycin-resistant cells and enhances resistance.
- The PI3K/AKT-mTOR pathway is involved in Cyclin L1-mediated Adriamycin resistance.

## Abstract

Chemoresistance is a common and thorny problem in the treatment of osteosarcoma (OS), which obstructs the response of relapse or metastasis of OS to chemotherapy and leads to the unfavorable prognosis of OS patients. Cyclin L1 (CCNL1) is a non-canonical cyclin that plays an important role in the regulation of tumor cell proliferation and lymph node metastasis. In this work, we explored the impact of CCNL1 expression levels on proliferation, migration, and Adriamycin (ADM) resistance in OS and related mechanisms. We found that CCNL1 expression levels were significantly associated with clinical prognosis of patients with OS and CCNL1 could promote OS proliferation and migration. In addition, we also revealed that cellular CCNL1 was significantly increased in ADM-resistant OS cells and promoted ADM resistance. The PI3K/AKT-mTOR pathway is involved in CCNL1-mediated ADM resistance in OS. In summary, CCNL1 is involved in the progression of ADM resistance and OS through the PI3K/AKT-mTOR pathway, which will provide a new clue to the mechanism of ADM resistance and a potential target for the treatment of ADM-resistant OS.