Your topics. New publications.

A compact browser notification when there’s something new. At most once a day — no account needed.

What interests you?

Optional and switchable off here at any time. We save your selected topics and device subscription; no email address is required. Privacy

Search the harborEN/DEAccount
Cellular senescence
Research brief

Review: SASP-mediated remodeling of the tumor microenvironment and cancer therapy

This review describes evidence that the senescence-associated secretory phenotype (SASP) can suppress or promote tumors depending on cellular and tissue condition, and discusses senolytics and senomorphics as emerging approaches. [1]

Automatic summary · not editorially reviewed

The key findings

  1. SASP comprises inflammatory cytokines, chemokines, growth factors and matrix-remodeling enzymes that regulate the tumor microenvironment. [1]

  2. Persistent SASP, particularly during therapy-induced senescence, can promote tumor growth, angiogenesis, immune evasion, cancer stemness, metastasis and therapeutic resistance. [1]

  3. SASP-associated molecules show potential as biomarkers, but specificity and tissue-dependent heterogeneity remain major challenges. [1]

The source at a glance

Study type / format
Narrative review (abstract only)
Population / context
Peer-reviewed English-language preclinical and clinical studies on cellular senescence, SASP, cancer and the tumor microenvironment, published primarily January 2000 to March 2026.
Summary based on
Study abstract
Original publication
September 1, 2026

SASP signals and tumor microenvironment remodeling

The review states that cellular senescence influences cancer through irreversible cell-cycle arrest, immune surveillance and paracrine signaling by SASP. SASP includes inflammatory cytokines, chemokines, growth factors and matrix-remodeling enzymes that regulate the tumor microenvironment. The authors describe current evidence on how SASP is induced and its condition-dependent roles in cancer.

Supporting source [1]

Transient versus persistent SASP in cancer progression

According to the review, SASP shows both tumor-suppressive and tumor-promoting activity depending on cellular and tissue condition. Transient SASP may enhance antitumor immunity and suppress early tumorigenesis. Persistent SASP, particularly during therapy-induced senescence, can promote tumor growth, angiogenesis, immune evasion, cancer stemness, metastasis and therapeutic resistance.

Supporting source [1]

Senolytics, senomorphics and biomarker challenges

The review reports that senolytics and senomorphics have emerged as promising approaches for targeting senescent cells and their detrimental secretory effects. SASP-associated molecules also show potential as biomarkers, although specificity and tissue-dependent heterogeneity remain major challenges. The authors conclude that understanding condition-dependent SASP functions is critical for developing effective senescence-targeted cancer therapies.

Supporting source [1]

How to interpret this

This is an abstract of a narrative review; the full text was not reviewed. The abstract reports literature searches but no pooled numbers, effect sizes or formal quality assessment. Statements about senolytics, senomorphics and biomarkers describe potential and challenges, not established human benefits.

Based on the study abstract; the full paper, tables and supplementary data were not reviewed.

Source & supporting passages

Read the quoted passagesIn the language of the original source
  1. Finding 1 ↑

    regulate the tumor microenvironment (TME)
  2. Finding 2 ↑

    persistent SASP, particularly during therapy-induced senescence (TIS)
  3. Finding 3 ↑

    specificity and tissue-dependent heterogeneity remain major challenges

AI-assisted summary with linked source passages. No independent editorial or clinical review.

Our editorial method

Discussion

Community discussions

0 topics

Member contributions. Share sources, disclose commercial interests, and avoid personal medical or dosing advice.

Loading…