PUM2 Promotes Glioblastoma Cell Proliferation and Migration via Repressing BTG1 Expression

Sun, Wei‐Zen; Yang, Jian; Yang, Liang; Li, Chen; Liu, Hongjiang; Liu, Xiaopeng; Jiao, Baohua

doi:10.1247/csf.18030

Cited by 20 publications

(18 citation statements)

References 25 publications

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“…PUM2 enhanced the stemness of breast cancer cells by interacting with NRP-1 (38). Knockdown of PUM2 suppressed the proliferation and invasion of glioblastoma cells by regulating BTG1 expression (42). Moreover, PUM2 has also been revealed to be involved in the progression of osteosarcoma (45).…”

Section: Discussionmentioning

confidence: 99%

“…Secondly, the predicted top 5 miRNAs were verified by luciferase reporter activity assay, and 3 miRNAs including PUM2 were revealed to be downregulated by miR-376a-3p. Thirdly, PUM2 was reported to promote cell proliferation and metastasis in several cancer types (38,42). However, the other 2 miRNAs were not reported to be involved in cancer pathology and were therefore not selected.…”

Section: Discussionmentioning

confidence: 99%

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LncRNA TTN‑AS1 promotes endometrial cancer by sponging miR‑376a‑3p

Shen

Yinyin

et al. 2020

Oncol Rep

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Increasing research has demonstrated that lncRNAs participate in the development of multiple cancer types. However, the role of TTN-AS1 in endometrial cancer (EC) remains unknown. The present study aimed to explore the function of titin-antisense RNA1 (TTN-AS1) in EC progression and the underlying mechanisms. qRT-PCR was performed to assess the TTN-AS1 expression patterns in EC tissues and cell lines. Loss of function experiments were carried out to estimate the effects of TTN-AS1 on EC cell proliferation, migration and invasion. To reveal the underlying mechanisms, informatics tools were used to predict the targets. Rescue experiments were performed to investigate the TTN-AS1-regulated miR-376a-3p/pumilio homolog 2 (PUM2) axis involved. The results of the present study revealed that TTN-AS1 was highly expressed in both EC tissues and cell lines, and TTN-AS1 knockdown inhibited EC cell proliferation, migration and invasion. With respect to the mechanisms, miR-376a-3p was revealed to be targeted by TTN-AS1, and reversed the effects on EC development induced by TTN-AS1. In addition, PUM2 was positively regulated by TTN-AS1, and miR-376a-3p mediated the regulation between them. Furtherly, in vivo experiments confirmed the results. Collectively, TTN-AS1 enhanced EC cell proliferation and metastasis by targeting the miR-376a-3p/PUM2 axis, which may shed light on EC diagnosis and treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

LncRNA TTN‑AS1 promotes endometrial cancer by sponging miR‑376a‑3p

Shen

Yinyin

et al. 2020

Oncol Rep

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“…Multiple studies have found associations between BTG1 and various tumors. It has been shown to be abnormally expressed in gastric cancer, kidney cancer, hepatocellular carcinoma, thyroid carcinoma, nasopharyngeal carcinoma, ovarian cancer, breast cancer, non-small cell lung cancer, glioblastoma and cervical cancer [10][11][12][13][14][15][16][17][18][19].…”

Section: Introductionmentioning

confidence: 99%

BTG1 inhibits malignancy as a novel prognosis signature in endometrial carcinoma

Huo

et al. 2020

Cancer Cell Int

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Background Endometrial carcinoma (EC) is one of the three major malignant tumors of the female reproductive system. In recent years, the incidence and mortality rate of EC have increased. B-cell translocation gene 1 (BTG1) is an anti-proliferation gene that regulates the occurrence and development of a variety of tumors, but there is no research regarding this gene in EC. Methods Based on The Cancer Genome Atlas (TCGA) database, we used a variety of bioinformatics tools and databases to explore the expression and prognosis of BTG1. We verified expression and prognosis of BTG1 in EC using qRT-PCR and analyzed the relevant clinicopathological parameters. We functionally enriched BTG1 and related genes in EC patients through the bioinformatics website and analyzed miRNA targets of BTG1 and interacting protein networks. Cell proliferation, wound healing, transwell invasion, and cell apoptosis assays were used to detect the effects of BTG1 on the malignant biological behavior of endometrial carcinoma cells (ECCs). The effect of BTG1 on the epithelial-to-mesenchymal transition (EMT) process was detected using western blot. Results We analyzed the expression and prognosis of BTG1 based on TCGA and found that low expression of BTG1 was associated with poor EC prognosis. The qRT-PCR suggested that BTG1 had low expression in EC. BTG1 expression was significantly correlated with overall survival (OS) shortening. Clinicopathological analysis suggested that expression of BTG1 was related to invasion depth and the International Federation of Gynecology and Obstetrics (FIGO) stage. EC pathological tissue type, fertility history, lymphatic metastasis, menopause, estrogen receptor (ER), progesterone receptor (PR), and age of diagnosis were not related. Functional enrichment analysis showed that BTG1 plays an important role in regulating embryonic development, tumorigenesis, apoptosis, and cell cycle. Biological behavior experiments suggest that BTG1 inhibits proliferation, migration, and invasion of ECCs, and promotes apoptosis of ECCs. Western blot indicated that BTG1 inhibited the EMT process of ECCs. Conclusions BTG1, as a tumor suppressor gene, plays an important role in the occurrence and development of EC. We believe that BTG1 can be used as a potential prognostic biomarker for EC.

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“…In fact, deregulated expression of Btg1 is involved in gastric (15), kidney (16), liver (17), thyroid (18), nasopharyngeal (19), ovarian (20), breast (21,22), and non-small-cell lung cancers (23), and is frequently associated with disease severity. Notably, although Btg1 is expressed in the developing and adult brain (11,(24)(25)(26), its involvement in brain tumors has been investigated only in gliomas (27,28).…”

Section: Introductionmentioning

confidence: 99%

Deletion of Btg1 Induces Prmt1-Dependent Apoptosis and Increased Stemness in Shh-Type Medulloblastoma Cells Without Affecting Tumor Frequency

et al. 2020

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About 30% of medulloblastomas (MBs), a tumor of the cerebellum, arise from cerebellar granule cell precursors (GCPs) undergoing transformation following activation of the Sonic hedgehog (Shh) pathway. To study this process, we generated a new MB model by crossing Patched1 heterozygous (Ptch1 +/− ) mice, which develop spontaneous Shh-type MBs, with mice lacking B-cell translocation gene 1 (Btg1), a regulator of cerebellar development. In MBs developing in Ptch1 +/− mice, deletion of Btg1 does not alter tumor and lesion frequencies, nor affect the proliferation of neoplastic precursor cells. However, in both tumors and lesions arising in Ptch1 +/− mice, ablation of Btg1 increases by about 25% the apoptotic neoplastic precursor cells, as judged by positivity to activated caspase-3. Moreover, although Btg1 ablation in early postnatal GCPs, developing in the external granule cell layer, leads to a significant increase of proliferation, and decrease of differentiation, relative to wild-type, no synergy occurs with the Ptch1 +/− mutation. However, Btg1 deletion greatly increases apoptosis in postnatal GCPs, with strong synergy between Btg1-null and Ptch1 +/− mutations. That pronounced increase of apoptosis observed in Ptch1 +/− /Btg1 knockout young or neoplastic GCPs may be responsible for the lack of effect of Btg1 ablation on tumorigenesis. This increased apoptosis may be a consequence of increased expression of protein arginine methyltransferase 1 (Prmt1) protein that we observe in Btg1 knockout/Ptch1 +/− MBs. In fact, apoptotic genes, such as BAD, are targets of Prmt1. Moreover, in Btg1-null MBs, we observed a two-fold increase of cells positive to CD15, which labels tumor stem cells, raising the possibility of activation of quiescent tumor cells, known for their role in long-term resistance to treatment and relapses. Thus, Btg1 appears to play a role in cerebellar tumorigenesis by regulating the balance between apoptosis and proliferation during MB development, also influencing the number of tumor stem cells.

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PUM2 Promotes Glioblastoma Cell Proliferation and Migration via Repressing BTG1 Expression

Cited by 20 publications

References 25 publications

LncRNA TTN‑AS1 promotes endometrial cancer by sponging miR‑376a‑3p

LncRNA TTN‑AS1 promotes endometrial cancer by sponging miR‑376a‑3p

BTG1 inhibits malignancy as a novel prognosis signature in endometrial carcinoma

Deletion of Btg1 Induces Prmt1-Dependent Apoptosis and Increased Stemness in Shh-Type Medulloblastoma Cells Without Affecting Tumor Frequency

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