PVT1 Promotes Cancer Progression via MicroRNAs

Wang, Wenxi; Zhou, Ruoyu; Wu, Yuwei; Liu, Yicong; Su, Wen; Wang, Xiong; Zeng, Zhaoyang

doi:10.3389/fonc.2019.00609

Cited by 90 publications

(73 citation statements)

References 68 publications

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“…Studies have suggested that patients with the BRAF V600E mutation should be overtreated to some extent [47], because BRAF mutations are an independent risk factor for lymph node metastasis and are closely related to tumor size and invasiveness [48][49][50][51][52][53][54][55][56][57]. Both the clinical studies and the basic medical studies performed here suggest that the presence of the BRAF mutation may lead to a decrease in the efficacy of iodine-131 treatment.…”

Section: Discussionmentioning

confidence: 72%

The BRAF V600E mutation is a predictor of the effect of radioiodine therapy in papillary thyroid cancer

Wang

et al. 2020

J. Cancer

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Objective: To investigate the correlation between the BRAF V600E gene mutation and clinicopathological features and thyroid function after iodine-131 treatment in patients with papillary thyroid cancer (PTC). Methods: A total of 128 PTC patients who underwent iodine-131 treatment after a total thyroidectomy from February 2015 to November 2016 at Hunan Cancer Hospital, China, were recruited. There were 25 males and 103 females. The age range was 11 to 73 years old. The BRAF V600E mutation in tumor tissues was detected by amplification-restriction mutation system polymerase chain reaction (ARMS-PCR), and the serum levels of Tg, TSH, Tg-Ab, and Tpo-Ab were measured by chemiluminescence after iodine-131 treatment. The BRAF V600E mutation was shown to be associated with clinicopathological characteristics and thyroid function indicators after iodine-131 treatment. Results: BRAF V600E mutation was detected in 75 of the 128 patients (58.6%) and was observed more frequently in cases with elevated Tg levels (Tg>1.00) at 3, 6, 12, and 18 months after treatment compared with patients without any BRAF mutations (P<0.05). Patients with BRAF V600E mutation had significant lower level of Tg-Ab at 3 and 12 months after treatment with iodine-131 than patients without BRAF V600E mutation (P<0.05). Among the 75 BRAF V600E patients, no significant association was found between the levels of TSH and Tpo-Ab after iodine-131 treatment (P>0.05). The BRAF V600E mutation was closely associated with the high-risk and age of the patient (≥45 years old) (P<0.05), but there was no significant correlation with gender, clinical stage, and distant metastasis. Conclusion:The BRAF V600E mutation is closely related to serum Tg elevation after treatment with iodine-131 in papillary thyroid cancer. These findings suggest that this BRAF mutation may be a predictor of the efficacy of iodine-131 treatment for papillary thyroid cancer.

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Section: Discussionmentioning

confidence: 72%

The BRAF V600E mutation is a predictor of the effect of radioiodine therapy in papillary thyroid cancer

Wang

et al. 2020

J. Cancer

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“…PVT1 can also serve as a potential predictor of cancer progression and patient prognosis [10,14,15]. Most studies have reported that PVT1 can promote proliferation, angiogenesis, apoptosis escape, and participate in DNA rearrangements, which might ultimately promote carcinogenesis [7,10,11,13,17,18]. However, recent studies have shown that PVT1, also a microRNA Host gene, can encode miR-1204, miR-1205, miR-1206, miR-1207-5p, miR-1207-3p, and miR-1208 [7,[19][20][21].…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA PVT1 interacts with MYC and its downstream molecules to synergistically promote tumorigenesis

Jin

Wang

Zhang

et al. 2019

Cell. Mol. Life Sci.

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Numerous studies have shown that non-coding RNAs play crucial roles in the development and progression of various tumor cells. Plasmacytoma variant translocation 1 (PVT1) mainly encodes a long non-coding RNA (lncRNA) and is located on chromosome 8q24.21, which constitutes a fragile site for genetic aberrations. PVT1 is well-known for its interaction with its neighbor MYC, which is a qualified oncogene that plays a vital role in tumorigenesis. In the past several decades, increasing attention has been paid to the interaction mechanism between PVT1 and MYC, which will benefit the clinical treatment and prognosis of patients. In this review, we summarize the coamplification of PVT1 and MYC in cancer, the positive feedback mechanism, and the latest promoter competition mechanism of PVT1 and MYC, as well as how PVT1 participates in the downstream signaling pathway of c-Myc by regulating key molecules. We also briefly describe the treatment prospects and research directions of PVT1 and MYC.

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“…MicroRNAs (miRNAs) belong to the family of non-coding RNAs with 20-24 nucleotides in length. Usually, miRNAs can silence the target genes by post-transcriptional regulation by binding to the 3 untranslated region (UTR) of target genes [6], and dysregulation of the miRNAs has been proved to have significant correlation with tumor initiation, progression and metastasis [7][8][9][10]. MiR-139-5p, located on chromosome 11q13.4, takes part in many important signaling pathway and has been showed to play anti-oncogenic roles in many cancers [11][12][13][14].…”

Section: Introductionmentioning

confidence: 99%

MiR-139-5p influences hepatocellular carcinoma cell invasion and proliferation capacities via decreasing SLITRK4 expression

et al. 2020

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The microRNA, miR-139-5p, has been proved to play important roles in regulating tumor progression, including prostate cancer, osteosarcoma, esophageal cancer, and so on, but its correlation of hepatocellular carcinoma (HCC) still remains unclear. Here we found that hsa-miR-139-5p (miR-139-5p) was decreased in HCC samples compared with normal liver tissues, and a lower expression of miR-139-5p was connected to a poorer prognosis. Mechanism study indicated that a decreased/increased miR-139-5p could increase/decrease HCC cells invasion and proliferation capacities via increasing SLITRK4 expression, what’s more, the reverse assays also confirmed the conclusion when we knocked down SLITRK4 in the miR-139-5p low-expression cells. Luciferase assay confirmed that miR-139-5p could directly bind to the 3′UTR of SLITRK4 mRNA to regulate its expression. Together, these findings show the importance of miR-139-5p/SLITRK4 pathway in HCC growth and progression and may provide new targets for us to better arrange the progression of HCC.

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PVT1 Promotes Cancer Progression via MicroRNAs

Cited by 90 publications

References 68 publications

The BRAF V600E mutation is a predictor of the effect of radioiodine therapy in papillary thyroid cancer

The BRAF V600E mutation is a predictor of the effect of radioiodine therapy in papillary thyroid cancer

Long non-coding RNA PVT1 interacts with MYC and its downstream molecules to synergistically promote tumorigenesis

MiR-139-5p influences hepatocellular carcinoma cell invasion and proliferation capacities via decreasing SLITRK4 expression

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