Inhibition of Nuclear Factor Kappa B as a Therapeutic Target for Lung Cancer

Altern Ther Health Med. 2022 Jan;28(1):44-51.

Abstract

Context: A wide variety of malignancies common to humans display abnormal constitutive expression of nuclear factor kappa beta (NF-κβ). The study of NF-κβ can increase understanding of its role in cancer, especially in lung-tumor formation.

Objective: This review intended to examine the research on the impact of the NF-κβ signaling pathway on the development of malignancies of the lungs and the advances in the regulation of that pathway to mitigate and provide treatment for lung carcinoma.

Design: The research team performed a narrative review by searching the PubMed, EMBASE, and Web of Science databases. The search used the keywords NF-κB or NF-kappa B or nuclear factor kappa B and non-small-cell lung cancer or non-small-cell lung carcinoma or NSCLC or lung cancer or lung adenocarcinoma or lung squamous carcinoma.

Setting: This study were conducted at Department of Respiratory and Critical Care Medicine, Qingxian People's Hospital, Cangzhou City, Hebei Province, People's Republic of China.

Results: As a major cell survival signal, nuclear factor-kappaB (NF-kappaB) is involved in multiple steps in carcinogenesis and in cancer cell's resistance to chemo- and radio-therapy. Recent studies with animal models and cell culture systems have established the links between NF-kappaB and lung carcinogenesis, highlighting the significance of targeting NF-kappa signaling pathway for lung cancer treatment and chemoprevention.

Conclusions: While no convincing evidence exists that survival of lung cancer cells is dependent on NF-κβ, inhibition of NF-κβ is a potent supporting therapy for enhancing the therapeutic effects of chemotherapy and radiotherapy. Constitutive and therapeutically induced activation of NF-κβ reduces the tumor-massacre effect of treatment, so inhibiting NF-κβ might increase antitumor activity.

Publication types

  • Review

MeSH terms

  • Animals
  • Carcinoma, Non-Small-Cell Lung* / drug therapy
  • Humans
  • Lung
  • Lung Neoplasms* / drug therapy
  • NF-kappa B / metabolism
  • Signal Transduction

Substances

  • NF-kappa B