The four-transmembrane protein MAL2 and tumor protein D52 (TPD52) are highly expressed in colorectal cancer and correlated with poor prognosis

Li, Jingwen; Li, Yongmin; He, Li; Liu, Yanlong; Cui, Binbin

doi:10.1371/journal.pone.0178515

Cited by 41 publications

(30 citation statements)

References 58 publications

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“…TPD52 is a tumor-promoting gene and is frequently overexpressed in multiple cancers, such as ovarian cancer, 37 prostate cancer, 38 colorectal cancer. 39 Due to the oncogenic role of TPD52 in many cancers, TPD52 should be further studied. Moreover, accumulating evidence revealed that TPD52 was involved in cellular transformation, proliferation, apoptosis, and metastasis.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of lncRNA PCAT6 Enhances Radiosensitivity in Triple-Negative Breast Cancer Cells by Regulating miR-185-5p/TPD52 Axis

Shi¹,

Wu²,

Liu³

et al. 2020

OTT

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Background: Long non-coding RNAs (lncRNAs) have been reported to play essential roles in regulating the radiosensitivity of cancers. Prostate cancer-associated transcript 6 (PCAT6) exerts oncogenic roles in several tumors. However, the roles of PCAT6 and its underlying mechanism in regulating the radiosensitivity of triple-negative breast cancer (TNBC) have not been investigated. Methods: The expression levels of PCAT6, microRNA-185-5p (miR-185-5p) and tumor protein D52 (TPD52) were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability, apoptosis and colony formation were assessed by Cell Counting Kit-8 (CCK-8) assay, flow cytometry and colony formation assay, respectively. The interaction between miR-185-5p and PCAT6 or TPD52 was predicted by bioinformatics analysis and verified by dual-luciferase reporter assay. Western blot was carried out to detect the protein level of TPD52. Results: PCAT6 and TPD52 were highly expressed and miR-185-5p was lowly expressed in TNBC tissues and cells, which was associated with an aggressive tumor phenotype in patients, affecting lymph node metastasis and clinical stage. PCAT6 or TPD52 knockdown or miR-185-5p overexpression enhanced the radiosensitivity of TNBC cells via inhibiting proliferation and inducing apoptosis. PCAT6 directly interacted with miR-185-5p and negatively regulated miR-185-5p expression. Moreover, TPD52 was confirmed as a target of miR-185-5p. Besides, PCAT6 regulated the radiosensitivity of TNBC cells through acting as a molecular sponge of miR-185-5p to modulate TPD52 expression. Conclusion: Knockdown of PCAT6 promoted the radiosensitivity of TNBC cells through regulating miR-185-5p/TPD52 axis, providing a vital theoretical basis to improve the radiotherapy efficiency of TNBC.

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Section: Discussionmentioning

confidence: 99%

Knockdown of lncRNA PCAT6 Enhances Radiosensitivity in Triple-Negative Breast Cancer Cells by Regulating miR-185-5p/TPD52 Axis

Shi¹,

Wu²,

Liu³

et al. 2020

OTT

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“…In that time, we have determined that the 19 kDa tetraspanning integral membrane protein, MAL2, is an important regulator of hepatic polarized protein sorting and have shown that it functions in basolateral secretion, basolateral membrane protein delivery and basolateral-to-apical transcytosis [3,4], but what is important to these studies is the finding that MAL2 expression is highly up-regulated up to 100-fold in a host of human cancers, including renal cell carcinoma, mesothelioma, neuroblastoma, cholangiocarcinoma, and cancers of the colon, liver, stomach, breast, ovary and pancreas [5][6][7][8][9][10][11][12][13][14]. High MAL2 expression has also been linked to bad prognosis in patients with colorectal or pancreatic cancer [5,13]. Genomic instability gains in chromosome 8q24 (where MAL2 resides) are associated with several epithelial cell-derived human cancers [15] and likely explains enhanced MAL2 transcript expression in at least a subset of these cancers.…”

Section: Introductionmentioning

confidence: 99%

MAL2-Induced Actin-Based Protrusion Formation is Anti-Oncogenic in Hepatocellular Carcinoma

López-Coral

Vecchio

Chahine

et al. 2020

Cancers

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Recent studies report that the polarity gene myelin and lymphocyte protein 2 (MAL2), is overexpressed in multiple human carcinomas largely at the transcript level. Because chromosome 8q24 amplification (where MAL2 resides) is associated with hepatocellular- and cholangio-carcinomas, we examined MAL2 protein expression in these human carcinoma lesions and adjacent benign tissue using immunohistochemistry. For comparison, we analyzed renal cell carcinomas that are not associated with chromosome 8q24 amplification. Surprisingly, we found that MAL2 protein levels were decreased in the malignant tissues compared to benign in all three carcinomas, suggesting MAL2 expression may be anti-oncogenic. Consistent with this conclusion, we determined that endogenously overexpressed MAL2 in HCC-derived Hep3B cells or exogenously expressed MAL2 in hepatoma-derived Clone 9 cells (that lack endogenous MAL2) promoted actin-based protrusion formation with a reciprocal decrease in invadopodia. MAL2 overexpression also led to decreased cell migration, invasion and proliferation (to a more modest extent) while loss of MAL2 expression reversed the phenotypes. Mutational analysis revealed that a putative Ena/VASP homology 1 recognition site confers the MAL2-phenotype suggesting its role in tumor suppression involves actin remodeling. To reconcile decreased MAL2 protein expression in human carcinomas and its anti-oncogenic phenotypes with increased transcript levels, we propose a transcriptional regulatory model for MAL2 transient overexpression.

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“…TPD52 is a coiled-coil motif-bearing protein that plays a regulatory role in tumor progression. Previous studies have shown the upregulated expression of TPD52 and its function as a tumor promoter in prostate cancer, 33 colorectal cancer, 34 lung squamous cell carcinoma, 35 and breast cancer. 24 Dasari et al 33 showed that TPD52 overexpression promotes the migration and proliferation of prostate cancer cells, while Kumamoto et al 35 revealed the suppressive effect of TPD52 knockdown on the migration and invasion of lung squamous cell carcinoma cells.…”

Section: Discussionmentioning

confidence: 97%

Long-Noncoding RNA FGD5-AS1 Enhances the Viability, Migration, and Invasion of Glioblastoma Cells by Regulating the miR-103a-3p/TPD52 Axis

Su¹,

Ji²,

Xue³

et al. 2020

CMAR

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Purpose: This study was designed to explore the functional role of FYVE, RhoGEF, and PH domain containing 5 antisense RNA 1 (FGD5-AS1) and the underlying regulatory mechanism in the progression of glioblastoma (GBM). Materials and Methods: FGD5-AS1 expression was analyzed in The Cancer Genome Atlas (TCGA), and then detected in GBM tissues and cells by quantitative reversetranscription polymerase chain reaction. Viability, migration, and invasion of GBM cells were assessed using the MTT, wound healing, and transwell assays, respectively. StarBase/ TargetScan analysis and dual-luciferase reporter gene (DLR) assay were performed to investigate the relationship between FGD5-AS1/tumor protein D52 (TPD52) and miR-103a-3p. A xenograft tumor model was established to evaluate the role of FGD5-AS1 in GBM tumorigenesis in vivo. Results: FGD5-AS1 was overexpressed in GBM tissues and cells, and silencing of FGD5-AS1 expression resulted in the inhibition of the viability, migration, and invasion of GBM cells. miR-130-3p was a target of FGD5-AS1, and its expression was negatively regulated by FGD5-AS1. Silencing miR-103a-3p expression resulted in the abrogation of the inhibitory effects of si-FGD5-AS1 on the viability, migration, and invasion of GBM cells. TPD52 was a target of miR-103a-3p and suppressed the antitumor effects of FGD5-AS1 silencing on GBM cells. In addition, FGD5-AS1 silencing inhibited the growth of xenograft tumors in vivo by modulating the miR-103a-3p/TPD52 axis. Conclusion: Silencing of FGD5-AS1 inhibited the viability, migration, and invasion of GBM cells by regulating the miR-103a-3p/TPD52 axis.

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The four-transmembrane protein MAL2 and tumor protein D52 (TPD52) are highly expressed in colorectal cancer and correlated with poor prognosis

Cited by 41 publications

References 58 publications

<p>Knockdown of lncRNA <em>PCAT6</em> Enhances Radiosensitivity in Triple-Negative Breast Cancer Cells by Regulating<em> miR-185-5p</em>/<em>TPD52</em> Axis</p>

<p>Knockdown of lncRNA <em>PCAT6</em> Enhances Radiosensitivity in Triple-Negative Breast Cancer Cells by Regulating<em> miR-185-5p</em>/<em>TPD52</em> Axis</p>

MAL2-Induced Actin-Based Protrusion Formation is Anti-Oncogenic in Hepatocellular Carcinoma

<p>Long-Noncoding RNA FGD5-AS1 Enhances the Viability, Migration, and Invasion of Glioblastoma Cells by Regulating the miR-103a-3p/TPD52 Axis</p>

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