Senescence in head and neck squamous cell carcinoma - relationship between senescence-associated secretory phenotype (SASP) mRNA expression level and clinicopathological features

Sep 21, 2026

Cellular senescence is a state marked by cell-cycle arrest and resistance to apoptosis. In cancer, senescence can be triggered by oncogenes or therapy, where persistent accumulation of senescent cells may promote carcinogenesis via the senescence-associated secretory phenotype (SASP). Gene expression of senescence markers (p16, LMNB1) and SASP factors (IL-6, IL-1b, CXCL-1, TNF-α) was assessed in head and neck squamous cell carcinoma tissues and related to clinical follow-up. Higher SASP factor levels were found in tumors versus normal tissues, and SASP expression correlated with clinicopathological features.

LanguageEnglish

CategoryResearch & Report

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Pages11

Reading Time28 min

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Abstract

Background

Material and methods

Results

Conclusion

Introduction

Cellular senescence and tumor biology

SASP factors and tumor microenvironment

Study rationale

Clinical and Translational Oncology (2024) 26:1022–1032 [https://doi.org/10.1007/s12094-023-03364-6](https://doi.org/10.1007/s12094-023-03364-6) Senescence in head and neck squamous cell carcinoma: relationship between senescence‑associated secretory phenotype (SASP) mRNA expression level and clinicopathological features Kamila Ostrowska1,2 · Patryk Niewinski1 · Igor Piotrowski2 · Julia Ostapowicz1,2,4 · Sabina Koczot1 · Wiktoria Maria Suchorska2,4 · Paweł Golusiński5 · Michal Mateusz Masternak1,3 · Wojciech Golusiński1 Received: 30 April 2023 / Accepted: 30 November 2023 / Published online: 4 January 2024 © The Author(s) 2024 Abstract Background Cellular senescence is a state characterized by cell-cycle arrest and apoptotic resistance. Senescence in cancer may be induced by oncogenes or therapy. While cellular senescence might play an important role in protection against cancer development, elevated and uncontrolled senescent cells accumulation may promote carcinogenesis by secreting a collection of pro-inflammatory factors, collectively termed the senescence-associated secretory phenotype (SASP) . Material and methods We determined the gene expression at mRNA level of selected cellular senescence markers (p16 and LMNB1) and SASP factors (IL-6, IL-1b, CXCL-1 and TNF-α) in 72 cancerous tissues and 64 normal tissues obtained from patients with head and neck squamous cell carcinoma (HNSCC) and correlated this data with patients’ clinical follow-up. Results Our results indicate higher levels of selected SASP factors in cancerous compared to normal tissues. We presented the relationship between SASP factors expression at the transcript level and the progression of the disease. Moreover, we proposed CXCL1 as a candidate biomarker differentiating normal tissues from cancerous ones and IL1b expression as a molecular factor related to increased TNM stage. Conclusion Our primary study indicates that SASP expression may be associated with some clinicopathological features. However, a more detailed study is needed to present specific role of senescence-related mechanism and SASPs especially in tumor therapy response and in relation to the patient’s immune system condition. Keywords Head and neck squamous cell carcinoma · Cellular senescence · Senescence-associated secretory phenotype · Biomarkers Abbreviations CRC Colorectal cancer CXCL1 C-X-C motif chemokine ligand 1 CCL C–C motif chemokine ligand EMT Epithelial–mesenchymal transition FDA Food and drug administrartion HNSCC Head and neck squamous cell carcinoma IL1b Interleukin 1b IL6 Interleukin 6 LMNB1 Lamin B1 OS Overall survival OSCC Oral squamous cell carcinoma p16 Cyclin-dependent kinase inhibitor 2A Kamila Ostrowska and Patryk Niewinski these authors contributed equally to this work. Extended author information available on the last page of the article RFS RT-qPCR SASP SMS TIS TME TNF-α Relapse free survival Real-time quantitative polymerase chain reaction Senescence-associated secretory phenotype Senescence-messaging secretome Therapy-induced Senescence Tumor microenvironment Tumor necrosis factor α Introduction Head and neck squamous cell carcinomas (HNSCCs) develop from the mucosal epithelium in the oral cavity, pharynx and larynx and are the 7th most common malignancies worldwide. HNSCC accounts for more than 660,000 new cases and 325,000 deaths annually [1] . HNSCC is characterized by various genetic and epigenetic mutations and the presence of different types of cells. In response to various intrinsic and extrinsic stimuli (especially radiotherapy or definitive chemoradiotherapy) cancer cells may enter a state of permanent growth arrest known as cellular senescence [2, 3] . The impact of cellular senescence on tumorigenesis is dictated by the cell or tissue of origin and may be cancer specific [4]. The presence of senescent cells may be protective for tissue by inhibiting cancer cells proliferation

FAQs

What is the biological role of cellular senescence in cancer according to the study?

Cellular senescence involves growth arrest and apoptotic resistance. While it may protect against cancer development, uncontrolled accumulation of senescent cells can contribute to carcinogenesis through SASP-related pro-inflammatory signaling.

Which genes and SASP factors were measured in tumor and normal tissues?

The study quantified mRNA expression of senescence markers p16 and LMNB1, and SASP factors IL-6, IL-1b, CXCL-1 (CXCL-1) and TNF-α in 72 cancerous and 64 normal tissues.

What clinicopathological associations did the results highlight?

SASP factors showed higher transcript levels in cancerous than in normal tissues. CXCL1 was proposed as a candidate biomarker distinguishing normal from cancer tissues, and IL1b expression was linked to increased TNM stage.

Sep 21, 2026

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