Partition-Defective 3 (PARD3) Regulates Proliferation, Apoptosis, Migration, and Invasion in Esophageal Squamous Cell Carcinoma Cells

Wang, Lei; Zhang, Haiping; Hasim, Ayshamgul; Tuerhong, Abuduaini; Hou, Zhichao; Abdurahmam, Ablajan; Sheyhidin, Ilyar

doi:10.12659/msm.903380

Cited by 11 publications

(6 citation statements)

References 30 publications

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“…CTNNA3 mediates cell adhesion (Janssens et al, 2001); when CTNNA3 was knocked down, CTNNA3-depleted cells showed abnormal skeleton (Stahn et al, 2016). In esophageal cancer, PARD3 overexpression promotes cell apoptosis, inhibits cell proliferation, and inhibits cell migration and invasion, whereas PARD3 silencing promotes cell proliferation and increases migration and invasion (Wang et al, 2017). PTPRM overexpression in small intestinal neuroendocrine tumor cell lines reduced cell growth and proliferation and induced apoptosis (Barazeghi et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Whole-Genome Resequencing to Study Brucellosis Susceptibility in Sheep

Zhang

et al. 2021

Front. Genet.

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Brucellosis is a zoonotic disease and a major public health problem. However, the genetic mechanism of brucellosis in sheep remains unclear. In this study, serum samples were collected from 6,358 sheep from the F2 population (Dorper sheep ♂ × Hu sheep ♀), and antibody levels were continuously measured at 14 days and 1, 2, 3, 4, 5, 6, 7, 8, 9, and 10 months after administration of brucellosis vaccine. Finally, 19 brucellosis-resistant group (BRG) sheep and 22 brucellosis-susceptible group sheep (BSG) were screened for whole-genome sequencing. Using the fixation index, Fisher’s exact test, and chi-square test, a total of 205 candidate SNP sites were identified. Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis suggested that 138 candidate genes were significantly enriched in adherens junction (CTNNA3, PARD3, and PTPRM), cell adhesion molecules (NLGN1, CNTNAP2, NCAM1, and PTPRM), salivary secretion (LOC101102109, PRKG1, and ADCY2), and hippo signaling pathway (CTNNA3, YAP1, and PARD3). These findings provide valuable molecular markers for brucellosis resistance breeding in sheep and novel insights into the genetic mechanism of brucellosis resistance.

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Section: Discussionmentioning

confidence: 99%

Whole-Genome Resequencing to Study Brucellosis Susceptibility in Sheep

Zhang

et al. 2021

Front. Genet.

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“…A loss of Par3 can promote tumor metastasis in breast cancer (23). In summary, Par3 serves as a tumor promoter in radiationinduced retinal carcinoma (74) and ovarian cancer (75) and a tumor suppressor in most other cancer types, including breast cancer (23,76,77), thyroid cancer (78), lung cancer (79-81), glioma (82), esophageal cancer (83,84), endometrioid endometrial carcinoma (85), cervical cancer (86), and pancreatic cancer (87). Interestingly, research has also shown that Par3 has dual functions in skin cancer (88)(89)(90) and prostate cancer (73,91), with both pro-oncogenic and tumor-suppressive functions (90).…”

Section: Dual Function Of Par3 Proteinmentioning

confidence: 99%

“…Par3 is reduced or lost in a variety of cancer tissues including cervical cancer (86), lung adenocarcinoma (80), thyroid tumor (78), and human breast cancer tissues (77). In addition, the overexpression of Par3 results in the inhibition of the proliferation of esophageal cancer cells and intrauterine membrane carcinoma cells (83,85) as well as the promotion of tumor cell apoptosis (83). Furthermore, a loss of Par3 leads to active proliferation in many tumor cells (23,75,78,80,85,88).…”

Section: Par3 In Tumor Suppressionmentioning

confidence: 99%

Dual Function of Par3 in Tumorigenesis

Yuan

et al. 2022

Front. Oncol.

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Cell maintenance and the establishment of cell polarity involve complicated interactions among multiple protein complexes as well as the regulation of different signaling pathways. As an important cell polarity protein, Par3 is evolutionarily conserved and involved in tight junction formation as well as tumorigenesis. In this review, we aimed to explore the function of Par3 in tumorigenesis. Research has shown that Par3 exhibits dual functions in human cancers, both tumor-promoting and tumor-suppressive. Here, we focus on the activities of Par3 in different stages and types of tumors, aiming to offer a new perspective on the molecular mechanisms that regulate the functions of Par3 in tumor development. Tumor origin, tumor microenvironment, tumor type, cell density, cell–cell contact, and the synergistic effect of Par3 and other tumor-associated signaling pathways may be important reasons for the dual function of Par3. The important role of Par3 in mammalian tumorigenesis and potential signaling pathways is context dependent.

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“…However, despite advances have been made in recent years in the complete resections of ESCC, the prognosis of patients remains unsatisfactory due to the high incidence of local and distant failure. 4,5 Therefore, seeking a new direction for the treatment of ESCC is critical to improve patient prognosis.…”

Section: Introductionmentioning

confidence: 99%

<p>Loss of miR-204-5p Promotes Tumor Proliferation, Migration, and Invasion Through Targeting YWHAZ/PI3K/AKT Pathway in Esophageal Squamous Cell Carcinoma</p>

Shen¹,

Chai²,

Luo³

et al. 2020

OTT

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MicroRNAs dysregulation has been confirmed in multiple malignancies. This paper reported the molecular mechanism of miR-204-5p in esophageal squamous cell carcinoma (ESCC). Methods: miR-204-5p expression in 30 ESCC tumor tissues and 10 normal tissues was downloaded from RNA-seq data. ESCC tissues/normal tissues of 97 ESCC patients were collected. TE-1 and KYSE510 cells were transfected by miR-204-5p mimic, inhibitor, siYWHAZ or their corresponding controls. The phenotype of cells was detected by CCK-8 assay, transwell experiment, and flow cytometry. Luciferase reporter gene assay and RNAbinding protein immunoprecipitation (RIP) were performed to verify the targeting relationship between miR-204-5p and YWHAZ. miR-204-5p and YWHAZ expression in tissues/cells was detected by qRT-PCR and Western blot. Xenograft tumor experiment was performed. Results: miR-204-5p expression was declined in ESCC patients and cells, which was indicated the poor outcome of patients. Compared with siNC group, TE-1 cells in miR-204-5p inhibitor group had higher OD450 value, less cell percentage in G1 phase, and more cell percentage in S phase, lower apoptosis percentage, and higher migration and invasion cell numbers. Moreover, KYSE510 cells of miR-204-5p mimic group showed lower OD450 value, more cell percentage in G1 phase and less cell percentage in S phase, higher apoptosis percentage, and lower migration and invasion cell numbers than control. YWHAZ was directly inhibited by miR-204-5p. Relative to siNC group, TE-1 cells of miR-inhibitor group exhibited higher YWHAZ protein expression, higher OD450 value, less cell percentage in G1 phase and more cell percentage in S phase, lower apoptosis percentage, higher migration and invasion cell numbers, and higher p-PI3K/PI3K and p-AKT/AKT protein expression, while siYWHAZ rescued the effects of miR-inhibitor. miR-204-5p up-regulation inhibited ESCC growth in vivo. Conclusion: miR-204-5p inhibits ESCC progression by targeted inhibition of YWHAZ/ PI3K/AKT.

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Partition-Defective 3 (PARD3) Regulates Proliferation, Apoptosis, Migration, and Invasion in Esophageal Squamous Cell Carcinoma Cells

Cited by 11 publications

References 30 publications

Whole-Genome Resequencing to Study Brucellosis Susceptibility in Sheep

Whole-Genome Resequencing to Study Brucellosis Susceptibility in Sheep

Dual Function of Par3 in Tumorigenesis

<p>Loss of miR-204-5p Promotes Tumor Proliferation, Migration, and Invasion Through Targeting YWHAZ/PI3K/AKT Pathway in Esophageal Squamous Cell Carcinoma</p>

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