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Updated: Jan 16, 2026

PIP-on-a-chip: A Label-free Study of Protein-phosphoinositide Interactions
Published on: July 27, 2017
Phosphoinositide dynamics in virus-associated malignancies
Mingchuan Li1, Wenbin Zhong1, Emilio Hirsch2
1Guangzhou Institute of Cancer Research, the Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou 510095, China; State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou 510095, China.
Abstract:
Virus-associated cancers, which account for ~15-20% of the global cancer burden, arise from infections with human oncoviruses. These viruses drive malignant transformation through diverse mechanisms but share common oncogenic features, including reprogramming host membrane signaling and trafficking. Such processes are tightly regulated by phosphoinositides (PPIn), essential organizers of membrane dynamics and signal transduction implicated in cancer development and progression. Oncoviruses exploit host PPIn metabolism to facilitate their replication and persistence, often leading to its dysregulation. In turn, this disruption can activate oncogenic signaling pathways that promote malignant transformation. In this review, we summarize how oncoviruses manipulate PPIn metabolism to sustain their life cycle and drive long-term interactions with host cells, ultimately contributing to tumorigenesis.
Insights
Human oncoviruses manipulate phosphoinositides (PPIn) metabolism to promote virus replication and cancer development. This review details how oncoviruses dysregulate PPIn, driving oncogenic signaling and tumorigenesis.
Area of Science:
- Oncology
- Virology
- Molecular Biology
Background:
- Virus-associated cancers represent a significant global health burden.
- Human oncoviruses cause cancer by altering host cell functions, particularly membrane signaling and trafficking.
- Phosphoinositides (PPIn) are critical regulators of membrane dynamics and signal transduction, crucial in cancer progression.
Purpose of the Study:
- To review how human oncoviruses manipulate phosphoinositide metabolism.
- To elucidate the role of PPIn dysregulation in oncovirus-driven tumorigenesis.
Main Methods:
- Literature review of studies on oncoviruses and phosphoinositide metabolism.
- Analysis of mechanisms by which oncoviruses alter host PPIn pathways.
- Synthesis of findings linking PPIn dysregulation to oncogenic signaling.
Main Results:
- Oncoviruses actively exploit and dysregulate host phosphoinositide metabolism.
- Altered PPIn metabolism by oncoviruses facilitates viral replication and persistence.
- This metabolic reprogramming activates oncogenic signaling pathways, promoting malignant transformation.
Conclusions:
- Oncoviruses utilize phosphoinositides as key targets to sustain their life cycle.
- Manipulation of PPIn metabolism by oncoviruses is a critical step in long-term host cell transformation and tumorigenesis.
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