Regulation of myosin activation during cell–cell contact formation by Par3-Lgl antagonism: entosis without matrix detachment

Wan, Qingwen; Liu, Jing; Zheng, Zongheng; Zhu, Huabin; Chu, Xiaogang; Dong, Zheng; Huang, Shuang; Du, Quansheng

doi:10.1091/mbc.e11-11-0940

Cited by 54 publications

(49 citation statements)

References 46 publications

(75 reference statements)

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“…Like RhoA activity, levels of phosphorylated myosin light chain 2 at Ser19 (pMLC2), a readout of contractile myosin downstream of ROCK I/II, were also higher in the majority of internalizing cells compared to the hosts ( Figure 3B). In most internalizing cells, pMLC2 was enriched in the cortex oriented away from cell-cell junctions, similar to previous reports [21,22], or occasionally in plaques adjacent to cell-cell junctions (data not shown). This pattern was consistently observed in entotic cell structures from a variety of tumor cell types (Supplementary information, Figure S4A and S4B), as well as from cells isolated from pleural exudates of a patient with metastatic breast cancer (Supplementary information, Figure S4A).…”

Section: Polarized Distribution Of Rho Activity and Contractile Actomsupporting

confidence: 91%

Induction of entosis by epithelial cadherin expression

et al. 2014

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Cell engulfment typically targets dead or dying cells for clearance from metazoan tissues. However, recent evidence demonstrates that live cells can also be targeted and that engulfment can cause cell death. Entosis is one mechanism proposed to mediate the engulfment and killing of live tumor cells by their neighbors, an activity often referred to as cell cannibalism. Here we report that the expression of exogenous epithelial cadherin proteins (E-or P-cadherin) in human breast tumor cells lacking endogenous expression of epithelial cadherins induces entosis and inhibits transformed growth. Entosis induced by cadherin expression is associated with the polarized distribution of Rho and Rho-kinase (ROCK) activity within entotic cells, which is dependent on p190A RhoGAP activity. ROCK inhibition or downregulation of p190A RhoGAP expression reduces entosis and increases the transformed growth of epithelial cadherin-expressing tumor cells. These data define new cell systems for the study of entosis, and identify entosis as a mechanism of cell cannibalism that is induced by the establishment of epithelial adhesion and inhibits transformed growth.

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Section: Polarized Distribution Of Rho Activity and Contractile Actomsupporting

confidence: 91%

Induction of entosis by epithelial cadherin expression

et al. 2014

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“…Other reports also suggested that Metallothionein 2A 124 and Par3-Lgl 125 could regulate entosis through the RhoA-ROCK pathway.…”

Section: Differential Ar Roles In 5 Types Of Pca Cell Deathmentioning

confidence: 96%

Androgen receptor (AR) positive vs negative roles in prostate cancer cell deaths including apoptosis, anoikis, entosis, necrosis and autophagic cell death

Wen

Niu

Lee

et al. 2014

Cancer Treatment Reviews

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Androgen/androgen receptor (AR) signaling plays pivotal roles in the prostate development and homeostasis as well as in the progression of prostate cancer (PCa). Androgen deprivation therapy (ADT) with anti-androgens remains as the main treatment of PCa, and it has been shown to effectively suppress PCa growth during the first 12–24 months. However, ADT eventually fails and tumors may re-grow and progress into the castration resistant stage. Recent reports revealed that AR might play complicated and even opposite roles in PCa progression that might depend on cell types and tumor stages. Importantly, AR may influence PCa progression via differential modulation of various cell deaths including apoptosis, anoikis, entosis, necrosis, and autophagic cell deaths. Targeting AR may induce PCa cell apoptosis, autophagic cell deaths and programmed necrosis, yet targeting AR may also suppress cell deaths via anoikis and entosis that may potentially lead to increased metastasis. These differential functions of AR in various types of PCa cell death might challenge the current ADT with anti-androgens treatment. Further detailed dissection of molecular mechanisms by which AR modulates different PCa cell deaths will help us to develop a better therapy to battle PCa.

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“…Hoechst 33342 (Invitrogen) was used for DNA staining. pLV-mU6-EF1-GFP vector (Biosettia, San Diego, CA, USA) was used for lentivirus-mediated stable knockdown of Lgl2 in MDCK cells, as previously described [37].…”

Section: Calcium Switch Assay Immunofluorescence and Quantificationmentioning

confidence: 99%