Tricellular tight junction protein LSR/angulin-1 contributes to the epithelial barrier and malignancy in human pancreatic cancer cell line

Kyuno, Takuro; Kyuno, Daisuke; Kohno, Takayuki; Konno, Takumi; Kikuchi, Satoshi; Arimoto, Chihiro; Yamaguchi, Hiroshi; Imamura, Masafumi; Kimura, Yasutoshi; Kondoh, Masuo; Takemasa, Ichiro; Kojima, Takashi

doi:10.1007/s00418-019-01821-4

Cited by 22 publications

(33 citation statements)

References 23 publications

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“…LSR is the key molecule of the three-cell contact in the normal cell epithelial barrier and cancer cell malignancies [10]. In endometrial cancer and human pancreatic cancer, it has been found that the loss of LSR can induce the migration, invasion, and proliferation of cancer cells [11]. At the same time, LSR can damage the invasive properties of bladder cancer cells [12].…”

Section: Introductionmentioning

confidence: 99%

LSR Promotes Cell Proliferation and Invasion in Lung Cancer

Zhang

2021

Computational and Mathematical Methods in Medicine

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The lipolysis-stimulated lipoprotein receptor (LSR) displays an important regulatory role in cancer. However, the association between LSR and lung cancer is still elusive. Here, the candidate oncogene LSR on Ch.9q was obtained and assessed by bioinformatics analysis of The Cancer Genome Atlas (TCGA) dataset of lung cancer. We conducted clinical pathology and survival analysis based on the lung cancer database. We assessed the biological effects of LSR in lung cancer cells on cell proliferation. Our data indicated that LSR was upregulated in lung cancer cells. Meanwhile, LSR was identified in this study to be a poor prognostic factor, and its high expression exhibited relations with grades, stages, and nodal metastasis status. Using in vitro analysis, our data revealed that LSR could promote lung cancer progression by regulating cell proliferation, migration, and invasion. In our study, our data demonstrated that LSR was a tumor promoter for lung cancer and was a potential biomarker and target for lung cancer prognosis and treatment.

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Section: Introductionmentioning

confidence: 99%

LSR Promotes Cell Proliferation and Invasion in Lung Cancer

Zhang

2021

Computational and Mathematical Methods in Medicine

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“…Angulin-1 was originally identified as a lipoprotein receptor (LSR) in the liver [51]. The expression of angulin-1 also correlates with colon, bladder, breast, pancreatic, ovarian, and endometrial cancers [106][107][108][109][110][111]. Recently, Hiramatsu et al, developed the functional monoclonal antibody against the extracellular region of human angulin-1 (anti-hLSR mAb (#1-25)) that crossreacted with mouse LSR.…”

Section: Antibodies Against Angulin-1mentioning

confidence: 99%

Tight Junction Modulating Bioprobes for Drug Delivery System to the Brain: A Review

et al. 2020

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The blood-brain barrier (BBB), which is composed of endothelial cells, pericytes, astrocytes, and neurons, separates the brain extracellular fluid from the circulating blood, and maintains the homeostasis of the central nervous system (CNS). The BBB endothelial cells have well-developed tight junctions (TJs) and express specific polarized transport systems to tightly control the paracellular movements of solutes, ions, and water. There are two types of TJs: bicellular TJs (bTJs), which is a structure at the contact of two cells, and tricellular TJs (tTJs), which is a structure at the contact of three cells. Claudin-5 and angulin-1 are important components of bTJs and tTJs in the brain, respectively. Here, we review TJ-modulating bioprobes that enable drug delivery to the brain across the BBB, focusing on claudin-5 and angulin-1.

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“…We previously reported that the downregulation of LSR triggered an increase in both the expression of the Hippo pathway transcription factor TEAD and YAP target gene amphiregulin ( AREG ), a known ligand for EGFR 14 . Recently, we showed that the upregulation of AREG was observed by knockdown of LSR in the human pancreatic cancer cell line HPAC and by the downregulation of LSR in the poorly differentiated pancreatic ductal adenocarcinomas (PDAC) 10 . Therefore, the decrease in LSR expression induces downregulation of the epithelial barrier function, resulting in the promotion of cancer cell malignancy, although the precise mechanisms are still unknown.…”

Section: Introductionmentioning

confidence: 99%

Translocation of LSR from tricellular corners causes macropinocytosis at cell–cell interface as a trigger for breaking out of contact inhibition

et al. 2021

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Withdrawal from contact inhibition is necessary for epithelial cancer precursor cells to initiate cell growth and motility. Nevertheless, little is understood about the mechanism for the sudden initiation of cell growth under static conditions. We focused on cellular junctions as one region where breaking out of contact inhibition occurs. In well‐differentiated endometrial cancer cells, Sawano, the ligand administration for tricellular tight junction protein LSR, which transiently decreased the robust junction property, caused an abrupt increase in cell motility and consequent excessive multilayered cell growth despite being under contact inhibition conditions. We observed that macropinocytosis essentially and temporarily occurred as an antecedent event for the above process at intercellular junctions without disruption of the junction apparatus but not at the apical plasma membrane. Collectively, we concluded that the formation of macropinocytosis, which is derived from tight junction‐mediated signaling, was triggered for the initiation of cell growth in static precancerous epithelium.

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Tricellular tight junction protein LSR/angulin-1 contributes to the epithelial barrier and malignancy in human pancreatic cancer cell line

Cited by 22 publications

References 23 publications

LSR Promotes Cell Proliferation and Invasion in Lung Cancer

LSR Promotes Cell Proliferation and Invasion in Lung Cancer

Tight Junction Modulating Bioprobes for Drug Delivery System to the Brain: A Review

Translocation of LSR from tricellular corners causes macropinocytosis at cell–cell interface as a trigger for breaking out of contact inhibition

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