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The CD44 variant induces K562 cell acquired with resistance to adriamycin via NF-κB/Snail/Bcl-2 pathway

Feng Fan1, Zhang Xiuwen2, Liu Yongyi1

  • 1The Fourth Affiliated Hospital of Jiangsu University, 20 Zhengdong Road, Zhenjiang 212001, China.

Medical Hypotheses
|November 7, 2018
PubMed

Insights

The CD44v16 variant enhances chemotherapy resistance in K562 cancer cells by activating the NF-κB/Snail/Bcl-2 pathway. This finding provides insights into acquired drug resistance mechanisms.

Area of Science:

  • Cancer Biology
  • Molecular Oncology

Background:

  • Chemotherapy resistance, both innate and acquired, is a major challenge in cancer treatment, often driven by gene mutations.
  • Alternative splicing of CD44 is linked to tumor development and multidrug resistance, but its precise role remains unclear.

Purpose of the Study:

  • To investigate the role of the CD44v16 variant in conferring adriamycin resistance to K562 cells.
  • To elucidate the molecular mechanisms underlying CD44v16-mediated drug resistance.

Main Methods:

  • Introduction of the CD44v16 gene into sensitive K562 cells using a lentiviral expression system.
  • Assessment of drug resistance index.
  • Real-time PCR and Western blot analysis to measure protein expression levels (p65, Bcl-2, Snail, IKKβ).

Main Results:

  • CD44v16 expression significantly increased the drug resistance index in K562 cells.
  • Elevated expression of p65, Bcl-2, Snail, and IKKβ was observed in CD44v16-positive cells compared to controls.
  • These findings suggest activation of the NF-κB/Snail/Bcl-2 pathway.

Conclusions:

  • CD44v16 confers acquired resistance to adriamycin in K562 cells.
  • The mechanism involves the activation of the NF-κB/Snail/Bcl-2 pathway.
  • This study lays the groundwork for further research into CD44v16's function in drug resistance.
Keywords:
AdriamycinCD44v16Drug resistanceK562

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