Interplay between endoplasmic reticulum stress and non-coding RNAs in cancer

Area of Science:

• Molecular Biology
• Cancer Biology
• Cellular Stress Response

Background:

• Cancer cells endure stress from mutations, hypoxia, and drug toxicity, leading to endoplasmic reticulum (ER) stress.
• ER stress activates the unfolded protein response (UPR) to manage unfolded proteins.
• Non-coding RNAs (ncRNAs) are critical in adapting to adverse conditions via gene expression regulation.

Purpose of the Study:

• To review ER stress-induced UPR signaling in carcinogenesis.
• To explore the reciprocal regulation between ER stress and ncRNAs in cancer.
• To provide insights into tumorigenesis and therapeutic strategies.

Main Methods:

• Literature review of ER stress, UPR, and ncRNA interactions in cancer.
• Analysis of signaling pathways involved in ER stress and UPR.
• Examination of ncRNA roles (miRNAs, lncRNAs, circRNAs) in cancer progression.

Main Results:

• UPR components regulate transcription and translation, including ncRNA expression, for cellular adaptation.
• Aberrant ncRNA expression is linked to tumor growth, metastasis, angiogenesis, and drug resistance.
• ER stress and ncRNAs mutually regulate each other, influencing cancer cell fate.

Conclusions:

• The interplay between ER stress and ncRNAs is vital for cancer cell survival and progression.
• Understanding these interactions offers potential for novel cancer treatment and prevention strategies.
• Targeting the ER stress-ncRNA axis may yield effective therapeutic interventions.