Overexpression of LASS2 inhibits proliferation and causes G0/G1 cell cycle arrest in papillary thyroid cancer

Huang, Liangliang; Cheng, Xiaoming; Yang, Xiaoli; Li, Taolang; Feng, Guoli; Tang, Yingqi; Yang, Yan

doi:10.1186/s12935-018-0649-1

Cited by 12 publications

(8 citation statements)

References 43 publications

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“…Western blotting analysis was performed as previously described 26. The primary antibodies against the following proteins used in the experiment were from commercial sources: anti-JAZF1 (ab80329; 1:200) and anti-p65 (ab16502; 1:2000), both purchased from Abcam; anti-Bcl-2 (#15071; 1:500) and anti-p-p65, both purchased from CST; anti-Bax (ET1603-34; 1:2000) purchased from Hangzhou HuaAn Biotechnology Co., Ltd.; anti-TAK1 (12330-2-AP; 1:500) purchased from Proteintech; anti-GAPDH (SC-365062; 1:800) purchased from Santa Cruz Biotechnology, Inc. (Dallas, TX, USA).…”

Section: Methodsmentioning

confidence: 99%

<p>JAZF1 Suppresses Papillary Thyroid Carcinoma Cell Proliferation and Facilitates Apoptosis via Regulating TAK1/NF-κB Pathways</p>

Huang¹,

Cai²,

Luo³

et al. 2019

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PurposeJuxtaposed with another zinc finger gene 1 (JAZF1) is involved in gluconeogenesis, insulin sensitivity, cell differentiation, lipid metabolism and inflammation, but its role in carcinoma remains inexplicit.Patients and methodsWe explored the JAZF1 expression in human papillary thyroid cancer (PTC) tissues, adjacent normal thyroid tissues and nodular goitre tissues, as well as Ki67 expression in PTC tissues, using immunohistochemistry staining. Western blotting and RT-qPCR were performed to explore the JAZF1 expression levels in Nthy-ori 3–1, BCPAP and TPC-1 cells. BCPAP cells overexpressing JAZF1 were constructed using an Adv-JAZF1-GFP recombinant adenovirus vector. Next, the cell proliferation assay, colony formation assay, cell cycle analysis, apoptosis and immunofluorescence were performed. The mRNA expression level of nuclear factor-κB p65 (NF-κB p65) was examined using RT-qPCR. The expression of Bcl-2, Bax, transforming growth factor beta-activated kinase 1 (TAK1), NF-κB p65 and NF-κB p-p65 were examined using Western blotting.ResultsThe expression of JAZF1 in human PTC tissues was downregulated compared with adjacent thyroid tissues or nodular goitre. Additionally, JAZF1 expression was associated with the location and lymph node metastasis of PTC. The expression level of JAZF1 had a negative correlation with Ki67 labelling index (LI). Compared to Nthy-ori 3–1 cells and TPC-1 cells, BCPAP cells expressed the lowest JAZF1. JAZF1 overexpressed significantly inhibited proliferation, caused G0/G1 cell cycle arrest and promoted apoptosis in BCPAP cells. Furthermore, JAZF1 overexpressed in BCPAP cells clearly upregulated the expression level of Bax protein, whereas decreased the expression of Bcl-2, TAK1, NF-κB but did not affect the mRNA or protein expression level of NF-κB p65.ConclusionJAZF1 inhibits proliferation and induces apoptosis in BCPAP cells by suppressing the activation of TAK1/NF-κB signalling pathways, suggesting that JAZF1 may serve as a reliable molecular marker in PTC.

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Section: Methodsmentioning

confidence: 99%

<p>JAZF1 Suppresses Papillary Thyroid Carcinoma Cell Proliferation and Facilitates Apoptosis via Regulating TAK1/NF-κB Pathways</p>

Huang¹,

Cai²,

Luo³

et al. 2019

OTT

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“…It has been reported that proliferation can be enhanced by knocking out Cers2 after sciatic nerve injury (20). Cers2, which is known as a cell proliferation inhibitor, may participate in G0/G1 cell cycle arrest as previous studies (21,22) described. The cell cycle arrest may via a p53-dependent pathway (23).…”

Section: Discussionmentioning

confidence: 77%

Endothelial cells promote the proliferation and migration of Schwann cells

Meng¹,

Zou²,

Xu³

et al. 2022

Ann Transl Med

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Background: After peripheral nerve injury, Schwann cells proliferate and migrate to the injured site, thereby promoting peripheral nerve regeneration. The process is regulated by various factors. Endothelial cells participate in the process via angiogenesis. However, the effects of endothelial cells on Schwann cellsare not yet known. The present study sought to evaluate whether endothelial cells accelerate Schwann cell proliferation and migration.Methods: We established a co-culture model of rat Schwann cells (RSC96s) and rat aortic endothelial cells (RAOECs), and studied the effects of endothelial cells on Schwann cells by evaluating changes in Schwann cell proliferation and migration and related multiple genes and their protein expressions in the co-culture model. Results:The results showed that increasing the proportion of endothelial cells in the co-culture model enhanced the proliferation. At days 1 and 3 following the co-culturing, the relative growth rates of the cocultured cells were 122.87% and 127.37%, respectively, which showed a significant increase in the viability compared to that of the RSC96s (P<0.05). In this process, the expression of Ki67 increased. The migration ability of Schwann cells was also enhanced. The migration capacity of Schwann cells was detected by woundhealing and Transwell assays. The results of the group with 15% of endothelial cells was significantly higher than the results of the other groups (P<0.0001 and P<0.05, respectively). Further, neuregulin 1 and glial fibrillary acidic protein increased the process of Schwann cell migration. Conclusions:The results showed that endothelial cells can promote the proliferation and migration of Schwann cells and participate in peripheral nerve regeneration.

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“…However, the cell proliferation and invasive ability decreased and the cell apoptosis increased upon the overexpression of the variants compared with the control, especially the T3 variant. which may be interpreted that the TLC domain of TMSG-1/LASS2, a characteristic domain of LASS family involved in the synthesis of ceramide, contributed partially to suppressing cell proliferation, invasive ability and promoting cell apoptosis [6, 19,20].…”

Section: Discussionmentioning

confidence: 99%

TMSG1/LASS2 inhibits cell proliferation, invasive ability through a novel transcriptional regulation way mediated by Homeodomain Running title: a novel transcription regulation role of TMSG1

Wang

Xia

et al. 2022

Preprint

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Background: TMSG1/LASS2 is emerging as an effective tumor suppressor as a transmembrane protein since it has been first cloned. We for the first time found by accident in our previous study TMSG1/LASS2 could be located in the nucleus, and it contained Homeodomain and nuclear localization signal (NLS). We aimed to investigate whether TMSG1/LASS2 possessed the function of transcription factor and identify the target genes regulated by the transcriptional regulation function of TMSG1/LASS2.Methods: We constructed and transfected three variants containing different functional domains of TMSG1/LASS2 to human prostate cancer cell PC-3M-1E8. Immunofluorescence was performed to detect the cellular localization of the three variants and identified its functional domain mediating it entering the nucleus. Chromatin immunoprecipitation (ChIP) associated with high-throughput sequencing was performed to select the target genes binding to TMSG1/LASS2 protein. Then we investigated the transcriptional regulation effect of TMSG1/LASS2 on one of the target genes Neural Proliferation, Differentiation and Control 1 (NPDC1) by dual-luciferase reporter system, and examined the expression of NPDC1 upon the overexpression or knockdown of TMSG1/LASS2, as well as the cell proliferation ability, apoptosis and cell cycle. Results: Immunofluorescence result revealed the variants deleted Homeodomain or NLS could not enter the nucleus. Neural Proliferation, Differentiation and Control 1 (NPDC1) gene, whose promoter fragment was obtained from ChIP using TMSG1/LASS2 antibody for further study. Dual-Luciferase reporter system revealed TMSG1/LASS2, as well as the variant with the deletion of NLS could enhance the transcription of NPDC1 promoter rather than the variant deleted Homeodomain. RT-qPCR and Western blot results demonstrated the gene and protein levels of NPDC1 were significantly increased upon TMSG1/LASS2 overexpression other than the variants without Homeodomain or NLS. Moreover, the level of NPDC1 were markedly decreased upon TMSG/LASS2 knockdown. Furthermore, the full length TMSG1/LASS2 was more able to inhibit cell proliferation, invasive ability and promote the cell apoptosis than the variants without Homeodomain or NLS. Conclusions: TMSG1/LASS2 could enter the nucleus to play transcription factor role mediated by its Homeodomain and NLS. TMSG1/LASS2 could promote the transcription and subsequent expression of NPDC1, one of its target genes. TMSG-1/LASS2 might inhibit cell proliferation, invasive ability, promote cell apoptosis and G0/G1 cell cycle arrest partially mediated by its Homeodomain and NLS. We for the first time propose a new transcriptional regulation function of TMSG1/LASS2 in addition to the known tumor suppressor function as a transmembrane protein.

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Overexpression of LASS2 inhibits proliferation and causes G0/G1 cell cycle arrest in papillary thyroid cancer

Cited by 12 publications

References 43 publications

<p>JAZF1 Suppresses Papillary Thyroid Carcinoma Cell Proliferation and Facilitates Apoptosis via Regulating TAK1/NF-κB Pathways</p>

<p>JAZF1 Suppresses Papillary Thyroid Carcinoma Cell Proliferation and Facilitates Apoptosis via Regulating TAK1/NF-κB Pathways</p>

Endothelial cells promote the proliferation and migration of Schwann cells

TMSG1/LASS2 inhibits cell proliferation, invasive ability through a novel transcriptional regulation way mediated by Homeodomain Running title: a novel transcription regulation role of TMSG1

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