Downregulation of LSD1 suppresses the proliferation, tumorigenicity and invasion of papillary thyroid carcinoma K1 cells

Kong, Lingling; Man, Dongmei; Zhang, Guoan; Cui, Wen

doi:10.3892/ol.2016.4244

Cited by 4 publications

(4 citation statements)

References 41 publications

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“…For example, microRNA-126 was found to be down-regulated in PTC tissues and cell lines, while its up-regulation could suppress cell proliferation, migration and invasion, and promote the apoptosis of PTC cells [28]. Up-regulated expression of lysine-specific demethylase 1 ( LSD1 ) has been detected in PTC cells, and its knockdown inhibited cell proliferation, tumorigenicity and invasion [29]. The growth and migration of PTC cells have been enhanced by the overexpression of hematopoietic pre-B cell leukemia transcription factor (PBX)-interacting protein ( HPIP ) [30].…”

Section: Discussionmentioning

confidence: 99%

Down-regulated HSDL2 expression suppresses cell proliferation and promotes apoptosis in papillary thyroid carcinoma

Zeng

Wang

et al. 2019

Bioscience Reports

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Papillary thyroid carcinoma (PTC) is the most common type of thyroid cancer. Hydroxysteroid dehydrogenase like 2 (HSDL2) can regulate lipid metabolism and take part in cell proliferation. The purpose of the present study was to explore functional role of HSDL2 gene in PTC. The expression of HSDL2 protein in PTC tissues was estimated using immunohistochemistry analysis (IHC). HSDL2 mRNA level was detected through quantitative real-time polymerase chain reaction (qRT-PCR). Effects of HSDL2 gene on cell proliferation and apoptosis were assessed using the shRNA method for both in vitro and in vivo experiments. Potential target genes of HSDL2 were determined via bioinformatics analyses and Western blotting. HSDL2 was up-regulated in PTC tissues and cell lines compared with the controls (all P<0.05). Inhibiting HSDL expression could suppress PTC cell proliferation and cycle, and promote apoptosis in vitro. In vivo, the knockdown of HSDL2 gene could significantly suppress tumor growth (all P<0.05). Furthermore, AKT3, NFATc2 and PPP3CA genes might be potential targets of HSDL2 in PTC. HSDL2 expression was increased in PTC tissues and cells, which could promote tumor progression in vitro and in vivo.

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Section: Discussionmentioning

confidence: 99%

Down-regulated HSDL2 expression suppresses cell proliferation and promotes apoptosis in papillary thyroid carcinoma

Zeng

Wang

et al. 2019

Bioscience Reports

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“…Elevated levels of LSD1 in a wide spectrum of malignancies including prostate cancer ( 12 ), colon cancer ( 17 ), lung cancer ( 18 ), liver cancer ( 19 ), and thyroid carcinoma ( 20 ) are highly correlated with lymph node metastasis and poor prognosis. Based on our finding that elevated levels of LSD1 were highly related to the grades of the bladder cancers ( 16 ), we hypothesized that LSD1 plays an oncogenic role in BCa development and/or progression.…”

Section: Resultsmentioning

confidence: 99%

LSD1 Promotes Bladder Cancer Progression by Upregulating LEF1 and Enhancing EMT

et al. 2020

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Epithelial-to-mesenchymal transition (EMT) is one of the important underlying molecular mechanisms for most types of cancers including bladder cancer. The precise underlying molecular mechanism in EMT-mediated bladder cancer progression is far from completed. LSD1, a histone lysine-specific demethylase, is known to promote cancer cell proliferation, metastasis, and chemoresistance. We found in this study that LSD1 is highly upregulated in bladder cancer specimens, especially those underwent chemotherapy, and the elevated levels of LSD1 are highly associated with bladder cancer grades, metastasis status, and prognosis. Inhibiting or knockdown LSD1 repressed not only EMT process but also cancer progression. Mechanistically, LSD1 complexes with β-catenin to transcriptionally upregulate LEF1 and subsequently enhances EMT-mediated cancer progression. More importantly, LSD1 specific inhibitor GSK2879552 is capable of repressing tumor progression in patient-derived tumor xenograft. These findings altogether suggest that LSD1 can serve as not only a prognostic biomarker but also a promising therapeutic target in bladder cancer treatment.

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“…KDM1A down-regulation can also suppress the invasive ability of PTC cell line K1, 38 but how KDM1A affects PTC cells remains unknown.…”

Section: Discussionmentioning

confidence: 99%

“…They showed that the PTC tissues had higher KDM1A expression than the paracancerous tissues. KDM1A down‐regulation can also suppress the invasive ability of PTC cell line K1, but how KDM1A affects PTC cells remains unknown.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of KDM1A suppresses tumour migration and invasion by epigenetically regulating the TIMP1/MMP9 pathway in papillary thyroid cancer

Zhang

Sun

Qin

et al. 2019

J Cellular Molecular Medi

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Epigenetic dysregulation plays an important role in cancer. Histone demethylation is a well‐known mechanism of epigenetic regulation that promotes or inhibits tumourigenesis in various malignant tumours. However, the pathogenic role of histone demethylation modifiers in papillary thyroid cancer (PTC), which has a high incidence of early lymphatic metastasis, is largely unknown. Here, we detected the expression of common histone demethylation modifiers and found that the histone H3 lysine 4 (H3K4) and H3 lysine 9 (H3K9) demethylase KDM1A (or lysine demethylase 1A) is frequently overexpressed in PTC tissues and cell lines. High KDM1A expression correlated positively with age <55 years and lymph node metastasis in patients with PTC. Moreover, KDM1A was required for PTC cell migration and invasion. KDM1A knockdown inhibited the migration and invasive abilities of PTC cells both in vitro and in vivo. We also identified tissue inhibitor of metalloproteinase 1 (TIMP1) as a key KDM1A target gene. KDM1A activated matrix metalloproteinase 9 (MMP9) through epigenetic repression of TIMP1 expression by demethylating H3K4me2 at the TIMP1 promoter region. Rescue experiments clarified these findings. Altogether, we have uncovered a new mechanism of KDM1A repression of TIMP1 in PTC and suggest that KDM1A may be a promising therapeutic target in PTC.

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Downregulation of LSD1 suppresses the proliferation, tumorigenicity and invasion of papillary thyroid carcinoma K1 cells

Cited by 4 publications

References 41 publications

Down-regulated HSDL2 expression suppresses cell proliferation and promotes apoptosis in papillary thyroid carcinoma

Down-regulated HSDL2 expression suppresses cell proliferation and promotes apoptosis in papillary thyroid carcinoma

LSD1 Promotes Bladder Cancer Progression by Upregulating LEF1 and Enhancing EMT

Knockdown of KDM1A suppresses tumour migration and invasion by epigenetically regulating the TIMP1/MMP9 pathway in papillary thyroid cancer

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