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Updated: Oct 19, 2025
Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
Published on: May 14, 2016
Loss of haspin suppresses cancer cell proliferation by interfering with cell cycle progression at multiple stages
Peiling Wang1,2, Xiangmei Hua2, Yang Sun2
1School of Pharmaceutical Science and Technology, Tianjin University, Tianjin, P. R. China.
Abstract:
Our recent studies have shown that haspin, a protein kinase imperative for mitosis, is engaged in the interphase progression of HeLa and U2OS cancer cells. In this investigation, we employed the Fucci reporter system and time-lapse imaging to examine the impact of haspin gene silencing on cell cycle progressions at a single-cell level. We found that the loss of haspin induced multiple cell cycle defects. Specifically, the S/G2 duration was greatly prolonged by haspin gene depletion or inhibition in synchronous HeLa cells. Haspin gene depletion in asynchronous HeLa and U2OS cells led to a similarly protracted S/G2 phase, followed by mitotic cell death or postmitotic G1 arrest. In addition, haspin deficiency resulted in robust induction of the p21CIP1/WAF1 checkpoint protein, a target of the p53 activation. Also, co-depleting haspin with either p21 or p53 could rescue U2OS cells from postmitotic G1 arrest and partially restore their proliferation. These results substantiate the haspin's capacity to regulate interphase and mitotic progression, offering a broader antiproliferative potential of haspin loss in cancer cells.
Insights
Loss of haspin, a protein kinase, disrupts cell division in cancer cells, causing prolonged S/G2 phases and cell death. Restoring p21 or p53 partially rescues proliferation, highlighting haspin
Area of Science:
- Cell Biology
- Molecular Biology
- Cancer Research
Background:
- Haspin (haspin, a protein kinase) is crucial for mitosis.
- Recent studies indicate haspin's involvement in the interphase progression of cancer cells (HeLa and U2OS).
Purpose of the Study:
- To investigate the role of haspin in cell cycle progression at a single-cell level.
- To determine the effects of haspin gene silencing on interphase and mitosis in cancer cells.
Main Methods:
- Utilized the Fucci reporter system for cell cycle tracking.
- Employed time-lapse imaging for real-time observation of cell behavior.
- Performed gene silencing (depletion) and inhibition of haspin.
- Analyzed cell cycle phases (S/G2), cell death, and checkpoint protein induction (p21CIP1/WAF1).
Main Results:
- Haspin depletion significantly prolonged the S/G2 phase duration in both synchronous and asynchronous HeLa and U2OS cells.
- Loss of haspin led to increased mitotic cell death and postmitotic G1 arrest.
- Haspin deficiency robustly induced the p21CIP1/WAF1 checkpoint protein, a downstream target of p53 activation.
- Co-depletion of haspin with p21 or p53 rescued U2OS cells from G1 arrest and partially restored proliferation.
Conclusions:
- Haspin plays a critical role in regulating both interphase and mitotic progression.
- Haspin loss induces cell cycle defects and activates p53-dependent checkpoints.
- Targeting haspin presents a potential antiproliferative strategy for cancer therapy.
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