Comparative proteomic profiling of human lung adenocarcinoma cells (CL 1–0) expressing miR‐372

Lai, Juo Hsin; She, Tzu Fang; Juang, Yu Min; Tsay, Yeou Guang; Huang, Angus; Yu, Sung-Liang; Chen, Jeremy J.W.; Lai, Chien Chen

doi:10.1002/elps.201100329

Cited by 16 publications

(13 citation statements)

References 42 publications

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“…Yu et al [ 11 ] identified miR-372 as a prognostic marker for the prediction of cancer relapse and survival in non-small cell lung cancer patients independent of stage or histological type. Furthermore, Lai et al [ 12 ] provided evidence that miR-372 may post-transcriptionally downregulate the large tumor suppressor homolog 2 in non-small cell lung cancer patients resulting in tumorigenesis and proliferation. However, the role of miR-372 in HCC has not been clear.…”

Section: Introductionmentioning

confidence: 99%

Low mir-372 expression correlates with poor prognosis and tumor metastasis in hepatocellular carcinoma

Wang

et al. 2015

BMC Cancer

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BackgroundRecent studies have shown that miR-372 plays important roles in hepatocellular carcinoma (HCC) progression. However, results have been conflicting regarding its expression levels and role in HCC.MethodsRT-PCR and in situ hybridization was used to evaluate miR-372 expression in HCC tissues and cell lines. The methylation status of neighboring CpG islands upstream of the miR-372 promoter was analyzed by methylation-specific PCR (MSP). Transfection of miR-372 mimic into HCC cell lines was used to evaluate cellular proliferation and invasion. Prognostic significance was analyzed by the Kaplan–Meier survival method and Cox regression.ResultsmiR-372 was expressed at lower levels in HCC tissues compared with controls and was related to tumor metastasis and poor prognosis. Hypermethylation of miR-372 was detected in HCC cell lines and tissues, and miR-372 expression was restored upon 5-aza-dCyd treatment. Upregulated expression by mir-372 mimic transfection inhibited proliferation and invasion capacity in HCC cells.ConclusionsmiR-372 may play an important role in hepatic carcinogenesis and may serve as a new target or method to detect and treat HCC in the future.

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Section: Introductionmentioning

confidence: 99%

Low mir-372 expression correlates with poor prognosis and tumor metastasis in hepatocellular carcinoma

Wang

et al. 2015

BMC Cancer

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“…LATS2 mutations are rare [17,18] but other mechanisms have been reported to cause down-regulation of its expression such as promoter hypermethylation [19] and micro-RNA regulation [20,21]. The relation between reduced LATS2 expression and lung cancer progression, and the underlying mechanisms remain unknown.…”

Section: Introductionmentioning

confidence: 99%

Aberrant large tumor suppressor 2 (LATS2) gene expression correlates with EGFR mutation and survival in lung adenocarcinomas

et al. 2014

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Background Large tumor suppressor 2 (LATS2) gene is a putative tumor suppressor gene with potential roles in regulation of cell proliferation and apoptosis in lung cancer. The aim of this study is to explore the association of aberrant LATS2 expression with EGFR mutation and survival in lung adenocarcinoma (AD), and the effects of LATS2 silencing in both lung AD cell lines. Methods LATS2 mRNA and protein expression in resected lung AD were correlated with demographic characteristics, EGFR mutation and survival. LATS2-specific siRNA was transfected into four EGFR wild-type (WT) and three EGFR mutant AD cell lines and the changes in LATS2 expression and relevant signaling molecules before and after LATS2 knockdown were assayed. Results Fifty resected lung AD were included (M:F = 23:27, smokers:non-smokers = 19:31, EGFR mutant:wild-type = 21:29) with LATS2 mRNA levels showed no significant difference between gender, age, smoking and pathological stages while LATS2 immunohistochemical staining on an independent set of 79 lung AD showed similar trend. LATS2 mRNA level was found to be a significant independent predictor for survival status (disease-free survival RR = 0.217; p = 0.003; Overall survival RR = 0.238; p = 0.036). siRNA-mediated suppression of LATS2 expression resulted in augmentation of ERK phosphorylation in EGFR wild-type AD cell lines with high basal LATS2 expression, discriminatory modulation of Akt signaling between EGFR wild-type and mutant cells, and induction of p53 accumulation in AD cell lines with low baseline p53 levels. Conclusions LATS2 expression level is predictive of survival in patients with resected lung AD. LATS2 may modulate and contribute to tumor growth via different signaling pathways in EGFR mutant and wild-type tumors.

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“…A recent study showed that miR-372 regulates cell cycle, apoptosis, invasion and proliferation in various human cancer [24]. Lai et al [25] found that miR-372 post-transcriptionally downregulated large tumor suppressor 2 in non-small cell lung cancer patients, thereby accelerating cancer development and proliferation of the malignant cells. However, the role of miR-372 in liver cancer is unclear.…”

Section: Discussionmentioning

confidence: 99%

LncRNA HULC regulates hepatocellular carcinoma cell proliferation, apoptosis and epithelial-mesenchymal transition via the miR-372/CXCR4 axis

Líu¹,

Zhou²,

Yang³

et al. 2020

Preprint

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Background: Hepatocellular carcinoma (HCC) is a lethal malignancy and a major public health concern worldwide. Considering the public health risk posed by HCC, it is necessary to elucidate the mechanisms underlying liver cancer progression in order to identify more therapeutic targets. In this study, we will elucidate the role of LncRNA HULC in regulating HCC cell proliferation, apoptosis and epithelial-mesenchymal transition (EMT) via the miR-372/CXCR4 axis. Material and Methods: Target genes were predicted using the online TargetScan database. Cell models of gene over-expression and silencing were established by transfection, and the mRNA and protein expression levels were measured by qRT-PCR and Western blotting, respectively. Cell viability, proliferation and apoptosis were measured by the CCK-8 assay, colony formation assay and Annexin V-FITC/PI staining, respectively. In situ protein expression in tissues was examined by immunohistochemical staining. Results: HULC and CXCR4 were upregulated and miR-372 was downregulated in HCC tissue and cells. TargetScan prediction and dual luciferase assay revealed that miR-372 can target HULC or CXCR4. Furthermore, HULC and CXCR4 enhanced the viability of HCC cells, whereas miR-372 had the opposite effect. Consistent with this, HULC and CXCR4 increased the proliferation of these cells and miR-372 showed an inhibitory effect. Furthermore, HULC and CXCR4 blocked apoptosis in liver cancer cells and miR-372 facilitated the same. Finally, HULC and CXCR4 promoted EMT, as indicated by E-cadherin downregulation and Vimentin upregulation, whereas miR-372 had the opposite effects. Conclusion: HULC upregulates CXCR4 in HCC cells by inhibiting miR-372, which in turn promotes the proliferation, inhibits the apoptosis and accelerates the EMT of HCC cells.

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Comparative proteomic profiling of human lung adenocarcinoma cells (CL 1–0) expressing miR‐372

Cited by 16 publications

References 42 publications

Low mir-372 expression correlates with poor prognosis and tumor metastasis in hepatocellular carcinoma

Low mir-372 expression correlates with poor prognosis and tumor metastasis in hepatocellular carcinoma

Aberrant large tumor suppressor 2 (LATS2) gene expression correlates with EGFR mutation and survival in lung adenocarcinomas

LncRNA HULC regulates hepatocellular carcinoma cell proliferation, apoptosis and epithelial-mesenchymal transition via the miR-372/CXCR4 axis

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