MiR-133b Acts as a Tumor Suppressor and Negatively Regulates TBPL1 in Colorectal Cancer Cells

Xiang, Kaimin; Li, Xiaorong

doi:10.7314/apjcp.2014.15.8.3767

Cited by 36 publications

(25 citation statements)

References 22 publications

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“…Some highly expressed miRs may function as oncogenes by repressing tumor suppressor genes, whereas lowly expressed miRs may function as tumor suppressors by negatively regulating oncogenes. In terms of CRC, abnormal expression of several miRs such as miR-27b, miR-133b, miR-124 have been reported (Ye et al, 2013;Zhang et al, 2013b;Xiang and Li, 2014). Additionally, Zhang et al (2013a) found that ectopic expression of miR-224 promoted CRC tumor cell proliferation, migration, and invasion in vitro.…”

Section: Introductionmentioning

confidence: 99%

Decreased expression of miR-874 and its tumor suppressive function in human colorectal cancer

Wang¹,

Xia²,

Bi³

2016

Genet. Mol. Res.

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ABSTRACT. Dysregulation of miRNAs is associated with cancer development and progression. For example, aberrant expression of miR-874 has been found in some types of cancer. However, miR-874 expression and its clinical significance in colorectal cancer (CRC) have not yet been explored. The aim of the current study was to explore the effects of miR-874 in CRC tumorigenesis and development. Quantitative reverse-transcription PCR was performed to evaluate miR-874 levels in CRC cell lines and in 135 pairs of primary human CRC specimens and adjacent noncancerous tissues. The association of miR-874 expression with clinicopathological factors and prognosis was also analyzed. Furthermore, the effects of miR-874 on the biological behavior of CRC cells in vitro were investigated. Our results revealed that miR-874 expression was significantly downregulated in CRC cancer tissues and cell lines. Decreased miR-874 expression was significantly associated with larger tumor size, deeper invasion depth, and advanced TNM stage in vivo. Additionally, low miR-874 expression in CRC was an independent predictor of poor survival. Moreover, overexpression of miR-874 inhibited cell proliferation, invasion, and migration, and promoted cell apoptosis of the SW620 CRC cell line in vitro. Taken together, these findings indicate that miR-874 may act as a tumor suppressor in CRC, and may serve as a novel therapeutic target for miR-based therapy.

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Section: Introductionmentioning

confidence: 99%

Decreased expression of miR-874 and its tumor suppressive function in human colorectal cancer

Wang¹,

Xia²,

Bi³

2016

Genet. Mol. Res.

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“…It is well known that each miRNA may regulate multiple gene targets. Previous studies have identified numerous target genes of miR-133b in a variety of tumor types; these genes include TBPL1, fibroblast growth factor receptor-1, specificity protein-1 and epidermal growth factor receptor (11,12,(18)(19)(20); thus suggesting that the roles of miR-133b in tumorigenesis may be cell-or tissue-specific. The present study demonstrated that miR-133b overexpression inhibited, whereas its suppression increased, endogenous S1PR1 protein expression in NPC cells.…”

Section: A B C D Discussionmentioning

confidence: 99%

“…In addition, miR-133b has been shown to be downregulated in colorectal cancer tissues, as compared with adjacent tissues (12), and has been found to inhibit the proliferation of colon cells by suppressing the TATA box-binding protein-like protein 1 (TBPL1) (12). Furthermore, miR-133b has been shown to inhibit the proliferation, migration and invasion of osteosarcoma cells, and promote their apoptosis (13).…”

Section: Introductionmentioning

confidence: 99%

miR-133b, a microRNA targeting S1PR1, suppresses nasopharyngeal carcinoma cell proliferation

Cheng

Wang

2016

Experimental and Therapeutic Medicine

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Abstract. MicroRNAs (miRs) are a class of short and non-coding RNA molecules, which function as either oncogenes or tumor suppressors in the development of various human cancers, including nasopharyngeal carcinoma (NPC). The aim of the present study was to investigate the expression of miR-133b in NPC tissue samples, as compared with adjacent normal tissues, and to examine its roles and underlying mechanisms. Analysis using reverse transcription-quantitative polymerase chain reaction demonstrated that miR-133b was downregulated in NPC tissue samples, as compared with adjacent tissues. In vitro experiments using NPC cell lines transfected with miR-133b mimics or antisense oligonucleotides further demonstrated that the overexpression of miR-133b mimics impaired, whereas knockdown of its expression promoted, the proliferation of NPC cells. Sphingosine-1-phosphate receptor 1 (S1PR1) was predicted to be a target of miR-133b. Luciferase reporter assays showed that miR-133b inhibited the protein expression of S1PR1 by targeting its 3'-untranslated region. Furthermore, western blot analysis demonstrated that miR-133B altered the regulation of the signal transducer and activator of transcription-3 (STAT3) signaling pathway and the expression of downstream proteins in NPC cells. Therefore, the results of the present study suggested that a previously unknown miR-133b/S1PR1 molecular network may regulate NPC progression.

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“…Though many risk factors have been reported to be related to the CRC occurrence, the detailed pathogenesis mechanism of CRC remains not fully understood. Therefore, it is urgent to explore the mechanisms underlying CRC progression for a better prevention and therapy (Xiang and Li, 2014). Besides as a molecular chaperone in ER, GRP78 is often overexpressed in tumor cells and plays an important role in tumor cell proliferation, angiogenesis, metastasis and resistance to apoptosis.…”

Section: Discussionmentioning

confidence: 99%

GRP78 Secreted by Colon Cancer Cells Facilitates Cell Proliferation via PI3K/Akt Signaling

Fu¹,

Yang²,

Wu³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Glucose regulated protein 78 (GRP78) is usually recognized as a chaperone in the endoplasmic reticulum. However, increasing evidence indicates that GRP78 can be translocated to the cell surface, acting as a signaling receptor for a variety of ligands. Since little is known about the secretion of GRP78 and its role in the progression of colon cancer we here focused on GRP78 from colon cancer cells, and purified GRP78 protein mimicking the secreted GRP78 was able to utilize cell surface GRP78 as its receptor, activating downstream PI3K/Akt and Wnt/β-catenin signaling and promote colon cancer cell proliferation. Our study revealed a new mode of action of autocrine GRP78 in cancer progression: secreted GRP78 binds to cell surface GRP78 as its receptor and activates intracellular proliferation signaling.

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MiR-133b Acts as a Tumor Suppressor and Negatively Regulates TBPL1 in Colorectal Cancer Cells

Cited by 36 publications

References 22 publications

Decreased expression of miR-874 and its tumor suppressive function in human colorectal cancer

Decreased expression of miR-874 and its tumor suppressive function in human colorectal cancer

miR-133b, a microRNA targeting S1PR1, suppresses nasopharyngeal carcinoma cell proliferation

GRP78 Secreted by Colon Cancer Cells Facilitates Cell Proliferation via PI3K/Akt Signaling

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