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Suijkerbuijk, S. J.

Publications and source records attributed to Suijkerbuijk, S. J..

4 recordsLinked to original sources

NucLogic: Logic-based geometric 3D nuclear segmentation for fast and robust analysis of challenging biological imaging data

Nuclear segmentation in 3D microscopy remains challenging, particularly for low signal-to-noise ratio (SNR) data from timelapse imaging, in vivo experiments, or dense tissue samples. Yet accurate 3D nuclear segmentation is a prerequisite for quantitative single-cell analysis, making this a key bottleneck for high-throughput study of challenging datasets. We present NucLogic, a fast and robust 3D nuclear segmentation algorithm that combines the maturity of 2D segmentation with geometric stitching rules based on nuclear shape, orientation, and intensity, to reconstruct accurate 3D volumes. NucLogic reliably segments challenging datasets including long-term timelapse imaging of organoids, and large dense structures such as the zebrafish brain. Benchmarked against other state-of-the-art segmentation tools, NucLogic matches F1 scores at high SNR, with increasing outperformance as SNR decreases. Importantly, segmentation completes at 20-50% of the computation time, with greater speed gains on larger images. Beyond segmentation, NucLogic includes an intuitive graphical user interface allowing non-experts to segment, quantify, and visualize 3D and 4D data. This enables easy quantification of cell numbers and integration of a variety of both cell-intrinsic properties, such as phenotype, morphology, and local environment metrics, including density and spatial interactions. Together, NucLogic makes quantitative 3D nuclear analysis of previously unmanageable datasets accessible to a broad research community.

cell biology↗

Mechanical regulation of cell fate transitions underlying colorectal cancer metastasis formation

Colorectal cancer (CRC) cells exhibit high plasticity and transition between different cellular states during the development of metastasis. Lgr5-expressing cancer stem cells fuel the growth of the primary tumor and metastasis, yet disseminated tumor cells arriving at the metastatic site are devoid of Lgr5 expression. It is currently unknown how CRC cell fate transitions are regulated during the metastatic process and how tumor cells give rise to metastatic lesions despite being Lgr5neg. Here, we show that the reprogramming of disseminating CRC cells is driven by mechanical interactions with the Collagen I-rich interstitial matrix. Collagen I-induced pulling forces are sensed by integrins and mechanosensitive calcium channels, which together direct the transition of CRC cells into a fetal-like state. The fetal-like state is maintained after reaching the blood circulation and promotes metastasis-initiation of disseminated CRC cells in the liver. Our findings indicate a key contribution of mechanical signals in controlling cell fate transitions that underlie the metastatic potential of CRC, involving an interplay between different mechanosensitive mechanisms.

cancer biology↗

Cell competition promotes metastatic intestinal cancer through a multistage process

Cell competition plays an instrumental role in quality control during tissue development and homeostasis. Nevertheless, cancer cells can exploit this process for their own proliferative advantage. In our study, we generated mixed murine organoids and microtissues to explore the impact of cell competition on liver metastasis. Unlike competition at the primary site, the initial effect on liver progenitor cells does not involve the induction of apoptosis. Instead, metastatic competition manifests as a multistage process. Initially, liver progenitors undergo compaction, which is followed by cell cycle arrest, ultimately forcing differentiation. Subsequently, the newly differentiated liver cells exhibit reduced cellular fitness, rendering them more susceptible to outcompetion by intestinal cancer cells. Notably, cancer cells leverage different interactions with different epithelial populations in the liver, using them as scaffolds to facilitate their growth. Consequently, tissue-specific mechanisms of cell competition are fundamental in driving metastatic intestinal cancer.

cancer biology↗

Active elimination of intestinal cells drives oncogenic growth in organoids

Competitive cell-interactions play a crucial role in quality control during development and homeostasis. Here we show that cancer cells use such interactions to actively eliminate wild-type intestine cells in enteroid monolayers and organoids. This apoptosis-dependent process boosts proliferation of intestinal cancer cells. The remaining wild-type population activates markers of primitive epithelia and transits to a fetal-like state. Prevention of this cell fate transition avoids elimination of wild-type cells and, importantly, limits the proliferation of cancer cells. JNK signalling is activated in competing cells and is required for cell fate change and elimination of wild-type cells. Thus, cell competition drives growth of cancer cells by active out-competition of wild-type cells through forced cell death and cell fate change in a JNK dependent manner.

cancer biology↗