PIM1 knockdown inhibits cell proliferation and invasion of mesothelioma cells

Mawas, Amany Sayed; Amatya, Vishwa Jeet; Suzuki, Rui; Kushitani, Kei; El-Din, Mouchira M. Mohi; Takeshima, Yukio

doi:10.3892/ijo.2017.3863

Cited by 14 publications

(10 citation statements)

References 31 publications

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“…Consistent with our expectations, we found that LMP1-induced increase in Pim1 expression indeed promoted proliferation of NPC cells. Our results were consistent with other lab findings that proved high Pim1 expression enhanced cancerous cell growth 1,30–32…”

Section: Discussionsupporting

confidence: 94%

<p>Epstein-Barr virus-encoded LMP1 regulated Pim1 kinase expression promotes nasopharyngeal carcinoma cells proliferation</p>

Ding

Yuan

Jia

et al. 2019

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Background Epstein–Barr virus-encoded LMP1 plays a critical role in the carcinogenesis of nasopharyngeal carcinoma (NPC), but the mechanism remains elusive. We aimed to analyze the expression and clinical pathological significance of provirus integration site for Moloney murine leukemia virus 1 (Pim1) in clinical NPC, and to elucidate the effect of LMP1 on Pim1 expression and its mechanism. Methods Immunohistochemical staining was used to detect the expression of Pim1 in clinical NPC tissues and control nasopharyngeal chronic inflammation (NPI) tissues, and the correlation between Pim1 and clinical parameters of NPC patients was analyzed. The LMP1 stable expression cell line CNE1-LMP1-OV was constructed through infecting the well-differentiated nasopharyngeal carcinoma cells CNE1 with LMP1 overexpressing lentivirus. Then the in vivo experiments were conducted. Results Among 89 NPC patients, 48 cases (53.93%) were positive for Pim1, while only one case was Pim1 positive in 15 NPI controls (6.67%). Pim1 expression was not correlated with gender, age, smoking status and clinical classification of NPC patients, but positively correlated with T, N and M classification. CNE1-LMP1-OV cell line was successfully established, which displayed a higher cell proliferation ability and Pim1 expression. NF-κB inhibitor PDTC, PKC inhibitor GF109203X and STAT3 inhibitor Stattic significantly attenuated LMP1-induced Pim1 expression, and while AP-1 inhibitor SR11302 showed no inhibitory effect. Interestingly, Pim1 inhibitor quercetagetin significantly inhibited the proliferation of CNE1-LMP1-OV cells. Conclusion LMP1 mediates Pim1 expression through NF-κB, PKC and STAT3 signaling, which promotes the proliferation of NPC cells and participate in the clinical progression of NPC.

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Section: Discussionsupporting

confidence: 94%

<p>Epstein-Barr virus-encoded LMP1 regulated Pim1 kinase expression promotes nasopharyngeal carcinoma cells proliferation</p>

Ding

Yuan

Jia

et al. 2019

OTT

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“…Johnson et al (22) found that a miR-137 mimic inhibited the proliferation, invasion, and migration of mesothelioma cells, and Williams et al (23) found that miR-13 reduced proliferation, and increased apoptosis and necrosis of mesothelioma cells by downregulating MCL1. Further, we demonstrated previously that miR-1 and miR-214 inhibited mesothelioma cell progression by suppressing PIM1 (11,24), and miR-182 and miR-183 promoted mesothelioma cell progression by suppressing FOXO1 (25).…”

Section: Discussionsupporting

confidence: 57%

Inhibition of miR‑18a‑3p reduces proliferation of mesothelioma cells and sensitizes them to cisplatin

et al. 2020

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Malignant pleural mesothelioma is a notorious human malignancy. Despite combination chemotherapy with cisplatin and pemetrexed, the majority of patients with advanced malignant pleural mesothelioma have a poor prognosis. MicroRNAs (miRNAs/miRs) are short non-coding RNAs that regulate various biological processes by binding to the 3'-untranslated region of target gene mRNAs and suppressing their expression. Since abnormal expression patterns of miRNAs are a common feature in human malignancies, a number of them have been researched as potential therapeutic targets. Our previous study demonstrated that microRNA-18a (miR-18a) is upregulated in mesothelioma cell lines compared with in non-neoplastic mesothelial tissues, but its function remains unclear. In the present study, miRNA inhibitor was transfected into mesothelioma cell lines and then analyzed various cellular functions. Mesothelioma cells transfected with the miR-18a inhibitor exhibited lower proliferation and migration rates compared with cells transfected with a negative control inhibitor in proliferation and wound scratch assays, respectively. Additionally, the present study revealed that downregulation of miR-18a increased mesothelioma cell apoptosis. In a chemosensitivity assay, transfection of the miR-18a inhibitor significantly increased the sensitivity of mesothelioma cells to cisplatin but not to pemetrexed. Therefore, miR-18a may be a potential therapeutic target for mesothelioma resistant to cisplatin. Materials and methods Mesothelioma cell lines. Four human mesothelioma cell lines were used in this study. Two cell lines (ACC-MESO1 and ACC-MESO4) were purchased from the RIKEN BioResearch Center (Tsukuba, Japan) (15) and the other two (CRL-5915 and CRL-5946) were purchased from the American Type Culture Collection. Cells were cultured with Roswell Park Memorial

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“…Pim1 is overexpressed in various tumours such as breast cancer and prostate cancer and promotes tumour progression by promoting cell proliferation, survival and inhibition of apoptosis . Moreover, Pim1 promotes cancer cells growth by enhancing the Warburg effect and promotes epithelial‐mesenchymal transition and oncogenesis . Therefore, miR‐24‐2 is likely to play a carcinogenic role by promoting the expression and function of Pim1 in liver cancer.…”

Section: Discussionmentioning

confidence: 99%

miR24‐2 accelerates progression of liver cancer cells by activating Pim1 through tri‐methylation of Histone H3 on the ninth lysine

Yang

Song

Meng

et al. 2020

J Cellular Molecular Medi

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Several microRNAs are associated with carcinogenesis and tumour progression. Herein, our observations suggest both miR24‐2 and Pim1 are up‐regulated in human liver cancers, and miR24‐2 accelerates growth of liver cancer cells in vitro and in vivo. Mechanistically, miR24‐2 increases the expression of N6‐adenosine‐methyltransferase METTL3 and thereafter promotes the expression of miR6079 via RNA methylation modification. Furthermore, miR6079 targets JMJD2A and then increased the tri‐methylation of histone H3 on the ninth lysine (H3K9me3). Therefore, miR24‐2 inhibits JMJD2A by increasing miR6079 and then increases H3K9me3. Strikingly, miR24‐2 increases the expression of Pim1 dependent on H3K9me3 and METTL3. Notably, our findings suggest that miR24‐2 alters several related genes (pHistone H3, SUZ12, SUV39H1, Nanog, MEKK4, pTyr) and accelerates progression of liver cancer cells through Pim1 activation. In particular, Pim1 is required for the oncogenic action of miR24‐2 in liver cancer. This study elucidates a novel mechanism for miR24‐2 in liver cancer and suggests that miR24‐2 may be used as novel therapeutic targets of liver cancer.

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PIM1 knockdown inhibits cell proliferation and invasion of mesothelioma cells

Cited by 14 publications

References 31 publications

<p>Epstein-Barr virus-encoded LMP1 regulated Pim1 kinase expression promotes nasopharyngeal carcinoma cells proliferation</p>

<p>Epstein-Barr virus-encoded LMP1 regulated Pim1 kinase expression promotes nasopharyngeal carcinoma cells proliferation</p>

Inhibition of miR‑18a‑3p reduces proliferation of mesothelioma cells and sensitizes them to cisplatin

miR24‐2 accelerates progression of liver cancer cells by activating Pim1 through tri‐methylation of Histone H3 on the ninth lysine

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