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J Thorac Oncol: miR-17 down-regulates LKB1, suggesting that NSCLC patients with poor prognosis can be treated with energy stress

 Last Update: 2021-05-20
 Source: Internet
 Author: User

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meta analysis study

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Recently, preclinical models have revealed the susceptibility of non-small cell lung cancer ( NSCLC ) with co-mutation of LKB1/KRAS to metabolic stress therapy.

NSCLC

The researchers used NSCLC cell lines with different combinations of KRAS mutations and LKB1 deletions, as well as patient-derived xenografts (PDX) with high miR-17 expression (L/miR17H) or low expression (L/miR17L) to evaluate the LKB1 pathway Damage and apoptotic response to metformin .

Metformin

The analysis results showed that miR-17 is an epigenetic regulator of LKB1 in NSCLC .

miR-17 is an epigenetic regulator of LKB1 in NSCLC.

Correlation between the expression level of miR-17 in PDX and the OS of tumor-derived patients

Metformin treatment can only induce apoptosis after miR-17 overexpression in LKB1 ^WT cell line and L ^WT /miR17H PDX cells.

^WT^WTmiR-17 is negatively correlated with the expression of LKB1, and emphasizes the prognostic role of miR-17 in LKB1 ^WT patients ^WT

All in all, the study found that miR-17 is an intermediary factor of LKB1 expression in NSCLC tumors .

miR-17 is the mediating factor of LKB1 expression in NSCLC tumors miR-17 is the mediating factor of LKB1 expression in NSCLC tumors

Original source:

Borzi Cristina, Ganzinelli Monica, Caiola Elisa et al.

org/10.
1016/j.
jtho.
2021.
04.
005" target="_blank" rel="noopener">LKB1 down-modulation by miR-17 identifies NSCLC patients with worse prognosis eligible for energy-stress based treatments

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