Interleukin-1 alpha and high mobility group box-1 secretion in polyinosinic:polycytidylic-induced colorectal cancer cells occur via RIPK1-dependent mechanism and participate in tumourigenesis.
Colorectal cancer
Damage-associated molecular patterns (DAMPs)
High mobility group box-1 (HMGB1)
Inflammation
Interleukin-1 alpha (IL-1α)
Journal
Journal of cell communication and signaling
ISSN: 1873-9601
Titre abrégé: J Cell Commun Signal
Pays: Netherlands
ID NLM: 101308338
Informations de publication
Date de publication:
Mar 2023
Mar 2023
Historique:
received:
31
03
2022
accepted:
18
04
2022
pubmed:
10
5
2022
medline:
10
5
2022
entrez:
9
5
2022
Statut:
ppublish
Résumé
Pathogenic infections have significant roles in the pathogenesis of colorectal cancer (CRC). These infections induce the secretion of various damage-associated molecular patterns (DAMPs) including interleukin-1 alpha (IL-1α) and high mobility group box-1 (HMGB1). Despite their implication in CRC pathogenesis, the mechanism(s) that modulate the secretion of IL-1α and HMGB1, along with their roles in promoting CRC tumourigenesis remain poorly understood. To understand the secretory mechanism, HT-29 and SW480 cells were stimulated with infectious mimetics; polyinosinic:polycytidylic acid [Poly(I:C)], lipopolysaccharide (LPS) and pro-inflammatory stimuli; tumour necrosis factor-alpha (TNF-α). IL-1α and HMGB1 secretion levels upon stimulation were determined via ELISA. Mechanism(s) mediating IL-1α and HMGB1 secretion in CRC cells were characterized using pharmacological inhibitors and CRISPR-Cas9 gene editing targeting relevant pathways. Recombinant IL-1α and HMGB1 were utilized to determine their impact in modulating pro-tumourigenic properties of CRC cells. Pharmacological inhibition showed that Poly(I:C)-induced IL-1α secretion was mediated through endoplasmic reticulum (ER) stress and RIPK1 signalling pathway. The secretion of HMGB1 was RIPK1-dependent but independent of ER stress. RIPK1-targeted CRC cell pools exhibited decreased cell viability upon Poly(I:C) stimulation, suggesting a potential role of RIPK1 in CRC cells survival. IL-1α has both growth-promoting capabilities and stimulates the production of pro-metastatic mediators, while HMGB1 only exhibits the latter; with its redox status having influence. We demonstrated a potential role of RIPK1-dependent signalling pathway in mediating the secretion of IL-1α and HMGB1 in CRC cells, which in turn enhances CRC tumorigenesis. RIPK1, IL-1α and HMGB1 may serve as potential therapeutic targets to mitigate CRC progression.
Identifiants
pubmed: 35534784
doi: 10.1007/s12079-022-00681-3
pii: 10.1007/s12079-022-00681-3
pmc: PMC10030748
doi:
Types de publication
Journal Article
Langues
eng
Pagination
189-208Subventions
Organisme : Institut Pengurusan dan Pemantauan Penyelidikan, Universiti Malaya
ID : GPF006C-2019
Organisme : Malaysia Toray Science Foundation
ID : STRG0069
Informations de copyright
© 2022. The International CCN Society.
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