# Highlighting the Role of DCLK1 in Tumor Invasion and Potential for Therapeutic Intervention

## TL;DR

This paper discusses how DCLK1 contributes to tumor invasion in head and neck cancer and its potential as a target for new therapies.

## Contribution

The paper highlights new molecular insights into DCLK1's role in HNSCC and its potential for small molecule targeting.

## Key findings

- DCLK1 is involved in invadopodium formation in HNSCC.
- Upregulation of DCLK1 is linked to poor prognosis in multiple cancers.
- Inhibiting DCLK1 may offer clinical benefits for HNSCC treatment.

## Abstract

Head and neck squamous cell carcinoma (HNSCC) accounts for nearly 5% of
global cancer deaths per year, with epidemiological studies suggesting an
expected 30% increase in cases by 2030 due to rising incidence of viral
infection (i.e. huma papilloma virus [HPV]). Treatment consists primarily of
surgical tumor removal accompanied by post-operative chemoradiation therapy;
however, disease recurrence is still an issue amongst 10–26% of patients.
Doublecortin-like kinase 1 (DCLK1) is a microtubule-associated protein with dual
kinase activity, and upregulation has been associated with poor prognosis in
multiple solid tumors. Recent studies by Arnold et al.
highlighted a definitive role of DCLK1 in HNSCC invadopodium formation and
function, and has elucidated its potential for small molecule targeting. This
commentary summarizes the molecular findings by Arnold et al.
and evaluates them in regard to the current standings of DCLK1 targeting,
emphasizing why inhibiting this molecule could be of clinical significance.