Positive and Negative Influences of Senescence on Therapy Response
A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".
Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 3458
Special Issue Editor
Special Issue Information
Dear Colleagues,
Cellular senescence is involved in many biological processes, such as development, tissue repair, tumor suppression, tumor promotion, and age-related diseases. Cellular senescence is caused by two major triggers: 1) shortened telomere length, which leads to replicative senescence; 2) endogenous or exogenous stress (e.g., DNA-damage), which leads to stress-induced senescence. Senescent cells are characterized by large and flat shapes, large nuclei and nucleoli, senescence-associated β galactosidase activity (SA-β-gal), and senescence-associated secretary phenotype (SASP). SASP factors include a wide variety of cytokines, chemokines, growth factors, and matrix metalloproteases. Therefore, SASP factors autocrinally and/or paracrinally influence cellular function and are thought to be the most important function among senescent cells’ role.
Tumor treatment such as irradiation and chemotherapy damages DNA in both tumor and normal cells. Severe DNA damage induces cell death. In contrast, constitutive mild or moderate DNA damage, which is not be repaired, seems to induce senescence. SASP factors released from senescent cells may affect the growth, differentiation, migration, signal transduction, and cell–cell communication of both tumor and normal cells in patients. However, there are many unknowns in this field of study. The questions are: What kind of SASP factors are secreted from senescent cells? How much are SASP factors secreted? Are the kinds and amounts of SASP factors dependent on the source of DNA damage (e.g., ionizing radiation vs. doxorubicin)? Which cells are prone to senescence? In addition, although the identification of a senescent-cell-specific biomarker is necessary to know the state of a patient’s senescent cells and to develop a therapy targeting cellular senescence, how can we identify it? Finally, many tumor cells lack the p53–p21 and p16–Rb axes, which are important pathways for inducing cellular senescence. Are these tumor cells induced into senescence independent of both axes by DNA damage? Or do senescent cells arising from normal cells affect tumor cells via SASP?
This Special Issue will highlight the effect of senescent cells, especially SASP, on tumor cells, covering both basic and preclinical aspects that advance our understanding of senescent cells in patients.
Dr. Tsukasa Oda
Guest Editor
Manuscript Submission Information
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Keywords
- cellular senescence
- SASP
- p53–p21 axis
- p16–Rb axis
- biomarker
- DNA damage
