Ville Paakinaho

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Assistant Professor (tenure track)

University of Eastern Finland
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Finland

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Ville Paakinaho is an Assistant Professor (tenure track) at the University of Eastern Finland. His research focuses on molecular mechanisms in prostate cancer, particularly the interactions of androgen and glucocorticoid receptors, as well as metabolic reprogramming in associated diseases. Recent publications also explore the role of SUMOylation and the impact of matrix stiffness on gene expression and cell plasticity in cancer cells. He contributes significantly to understanding the transcriptional responses and signaling pathways that influence cancer development and progression.

Recent Grants

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Drug resistance-induced reprogramming of chromatin and transcription factor activity in prostate cancer

Open Date: 2021-09-01

Close Date: 2026-08-01

Grant: Close

Drug resistance-induced reprogramming of chromatin and transcription factor activity in prostate cancer (funding for research costs)

Open Date: 2021-09-01

Close Date: 2024-12-01

Grant: Close

Reprogramming Chromatin Occupancy and Transcriptional Activity by Dynamic Transcription Factor Transitions

Open Date: 2018-01-09

Close Date: 2021-08-31

Positions (1)

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Ville Paakinaho

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University of Eastern Finland

Postdoctoral Researcher in Cell or Molecular Biology, Prostate Cancer Therapy Resistance

The University of Eastern Finland is inviting applications for a Postdoctoral Researcher position in cell biology / molecular biology at the Institute of Biomedicine, Faculty of Health Sciences on the Kuopio Campus in Finland. The project, “Principles of pioneer transcription factor function in the development of prostate cancer therapy resistance” , is funded by the Research Council of Finland and led by Assistant Professor Ville Paakinaho . The research investigates how pioneer transcription factors change during the development of drug resistance in prostate cancer and how these processes are modulated by signal-dependent transcription factors and coregulators. The work uses state-of-the-art genome-wide sequencing , chromatin proteomics , imaging technologies , and functional perturbation approaches. The project also involves international mobility and collaboration, making it a strong fit for candidates interested in translational cancer biology, transcription factor biology, and advanced molecular methods. Eligibility highlights: applicants must hold a doctoral degree in cell biology, molecular biology, molecular medicine, or a related field; the PhD must normally have been completed within the last five years (with standard exclusions such as parental leave and military service). A strong research record and excellent/very good English skills are required. Experience in fluorescence imaging and genome editing of mammalian cells is an advantage, as are first-author peer-reviewed publications. Funding and terms: this is a fixed-term, full-time postdoctoral appointment for 3 years starting 1 September 2026 (or as agreed). Salary follows the Finnish university salary system, with a starting monthly salary of approximately EUR 3,560–4,050 depending on the personal salary element. Application deadline: 4 August 2026. Apply via the electronic application form and include the requested attachments: CV, publication list, degree certificates, language proficiency certificates if applicable, motivation letter, and a development plan. For more information, contact Ville Paakinaho at [email protected] .

2 months ago

Articles (22)

SIX2 promotes cell plasticity via Wnt/β-catenin signalling in androgen receptor independent prostate cancer

The use of androgen receptor (AR) inhibitors in prostate cancer gives rise to increased cellular lineage plasticity resulting in resistance to AR-targeted therapies. In this study, we examined the chromatin landscape of AR-positive prostate cancer cells post-exposure to the AR inhibitor enzalutamide. We identified a novel regulator of cell plasticity, the homeobox transcription factor SIX2, whose motif is enriched in accessible chromatin regions after treatment. Depletion of SIX2 in androgen-independent PC-3 prostate cancer cells induced a switch from a stem-like to an epithelial state, resulting in reduced cancer-related properties such as proliferation, colony formation, and metastasis both in vitro and in vivo. These effects were mediated through the downregulation of the Wnt/β-catenin signalling pathway and subsequent reduction of nuclear β-catenin. Collectively, our findings provide compelling evidence that the depletion of SIX2 may represent a promising strategy for overcoming the cell plasticity mechanisms driving antiandrogen resistance in prostate cancer.

Year:

2024

Collaborators (12)

Tapio Visakorpi

-

FINLAND

Markku Varjosalo

University of Helsinki

FINLAND

Christopher Jarzynski

Distinguished University Professor

University of Maryland at College Park

UNITED STATES

Jorma Palvimo

Professor of Medical Biochemisty

University of Eastern Finland

FINLAND

Lorenzo Rinaldi

Head of Translational Science

-

UNITED STATES

Gordon Hager

Chief

National Cancer Institute

UNITED STATES

Karolien De Bosscher

Full professor

-

BELGIUM

Sonia Kung

-

CANADA

Daniel Wüstner

University of Southern Denmark

DENMARK

Liza Dewyse

Vrije Universiteit Brussel

BELGIUM

Einari Niskanen

University Lecturer at University of Eastern Finland

University of Eastern Finland

FINLAND

Kirsi Ketola

University of Eastern Finland

FINLAND
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