PTEN in kidney cancer: A review and meta-analysis

Que, Wancai; Qiu, Hongqiang; Chen, Yu; Liu, Maobai; Wu, Chaoyang

doi:10.1016/j.cca.2018.01.031

Cited by 39 publications

(32 citation statements)

References 50 publications

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“…25 In addition, the decrease of PTEN is related to the poor survival outcome of renal cancer patients, PTEN plays a role in the occurrence and development of renal cancer. 26 Apoptosis-related gene Bax interacts with Bcl-2 to form a heterodimer or with itself to form a homodimer, and the increase in Bax homodimer often leads to apoptosis. 27 Bax upregulated and Bcl-2 downregulated can promote the apoptosis of melanoma skin cancer cells.…”

Section: Discussionmentioning

confidence: 99%

<p>MiR-29b-3p Reverses Cisplatin Resistance by Targeting COL1A1 in Non-Small-Cell Lung Cancer A549/DDP Cells</p>

Jia¹,

Wang²

2020

CMAR

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Objective: To investigate the expression of miR-29b-3p in tissues and cells of non-small-cell lung cancer (NSCLC) and its effect on cisplatin resistance in NSCLC cells and its mechanism. Methods: The mRNA expression of miR-29b-3p and COL1A1 in NSCLC tissue, cell line A549 and cisplatin-resistant cell line A549/DDP was detected by Mimics was transfected into A549/DDP cells, and the cell viability, proliferation, apoptosis and related protein expression were detected by CCK-8, flow cytometry and Western blot. Also, luciferase reporter gene assay was used to verify the targeting relationship between miR-29b-3p and COL1A1. Moreover, COL1A1 overexpression lentivirus and miR-29b-3p mimics (Mimics+COL1A1) were simultaneously transfected into A549/DDP cells, and then the cell viability and related protein expression were measured. Results: In NSCLC tissue and its cell line, miR-29b-3p was downregulated and COL1A1 was upregulated (P<0.05). After A549/DDP cell was transfected by mimics, its cell viability and proliferation rate decreased, apoptosis rate and the expression of tumor suppressor gene PTEN and apoptosis-related protein BAX were increased (P<0.05), which could be reversed by Mimics+COL1A1 co-transfection. Luciferase reporter gene assay indicated that COL1A1 was the target gene of miR-29b-3p. Conclusion: All in all, miR-29b-3p can reverse the cisplatin resistance of A549/DDP cells by inhibiting the expression of COL1A1 gene and increasing the expression of PTEN and BAX.

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Section: Discussionmentioning

confidence: 99%

<p>MiR-29b-3p Reverses Cisplatin Resistance by Targeting COL1A1 in Non-Small-Cell Lung Cancer A549/DDP Cells</p>

Jia¹,

Wang²

2020

CMAR

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“…Phosphatase and tensin homologue deleted on chromosome 10 (PTEN), also known as mutated in multiple advanced cancers (MMAC), was identified in 1997 by two independent research groups as a candidate tumor suppressor gene that was located at the human chromosome 10q23, a site frequently damaged in primary human malignancies (13,14). The loss of PTEN function can occur via a series of genetic or epigenetic abnormalities, such as point chromosomal deletions, mutations, promoter hypermethylation and post-translational modifications (15,16), and may result in various human malignancies, including renal cancer (17), pancreatic cancer (18), glioma (19), colorectal cancer (20), breast cancer (21), endometrial cancer (22), melanoma (23) and myeloid malignancies (24).…”

Section: Introductionmentioning

confidence: 99%

Expression and clinical correlation of Survivin and PTEN in gastric cancer patients

et al. 2020

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Reports on the correlation between the expression of Survivin/phosphatase and tensin homolog (PTEN) proteins and clinical factors in gastric cancer (GC) are varied, and the sample sizes were also not sufficient. The present study aimed to detect the expression of Survivin and PTEN proteins in GC patients on the basis of a greater number of specimens and to analyze the correlation with clinical features and survival. The results revealed that the Survivin expression rates in GC, normal tissues and metastatic lymph nodes were 72% (232/322), 5% (6/120) and 80% (36/45), respectively, while the PTEN expression rates were 34% (109/322), 92.5% (111/120) and 24.4% (11/45), respectively, and the differences between cancer and normal tissue or metastatic lymph nodes were significant for both proteins (P<0.05). The expression of Survivin was significantly associated with gross type, depth of invasion, distant metastasis, tumor, necrosis and metastasis (TNM) stage and vascular invasion, while PTEN expression was predominantly associated with age, tumor size, invasion depth, TNM stage and lymphatic invasion in GC patients (P<0.05). The expression of both was associated with postoperative metastasis and metastatic site (P= 0.007 and P= 0.011 for Survivin, and P= 0.002 and P= 0.005 for PTEN). There was a negative association between the expression levels of Survivin and PTEN (P= 0.001, r=-0.524). The expression levels of both were also associated with prognosis. The expression of Survivin and PTEN protein exhibit opposing trends in GC, which may indicate adverse biological effects in the occurrence of GC. The Survivin and PTEN expression levels are likely to be an important molecular event in gastric tumorigenesis and may be considered as molecular markers of GC progression and reliable prognostic indicators of GC.

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“…A number of studies have investigated Burkitt's lymphoma; however, the specific pathogenesis of the disease is not fully understood. Our previous studies found that inhibition of the PI3K pathway can inhibit the proliferation of Burkitt's lymphoma, and abnormal expression of phosphatase and tensin homolog (PTEN) is common in solid tumors, including breast cancer, kidney cancer, esophageal cancer, endometrial cancer (6)(7)(8) and diffuse large B cell lymphoma (12). Therefore, a relationship between PTEN overexpression and the incidence of Burkitt's lymphoma has been indicated.…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, PTEN has been indicated to negatively regulate the PI3K/AKT signaling pathway. As a negative regulatory factor, PTEN exhibits mutations, deletions, methylation and abnormal activity in solid tumors (6)(7)(8). PTEN is also abnormally expressed in B-cell lymphomas, including diffuse large B-cell lymphoma (9), resulting in the aberrant activation of the PI3K/AKT pathway.…”

Section: Introductionmentioning

confidence: 99%

Role and mechanism of PTEN in Burkitt's lymphoma

Xin

et al. 2020

Oncol Rep

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The aim of the present study was to explore the possible mechanisms of phosphatase and tensin homolog (PTEN) in the pathogenesis of Burkitt's lymphoma, and provide novel information that can be used in the targeted treatment of this disease. PTEN lentiviral overexpression vector and short-hairpin PTEN silencing vectors were constructed. The effect of PTEN on the growth and proliferation of CA46 and RAJI cells was analyzed using a Cell Counting Kit-8 assay. Apoptosis was detected by Hoechst 33342 and propidium iodide double staining. Flow cytometry was used to analyze the cell cycle. A Transwell chamber was used to detect cell migration and invasion abilities. Western blot analysis was used to detect related protein changes. The mechanism of the effect of PTEN on the biological characteristics of Burkitt's lymphoma cells was subsequently analyzed. The results revealed that PTEN inhibited the proliferation of CA46 and RAJI cells by downregulating the expression of p-AKT, It was indicated that the upregulation of proapoptotic proteins (including Bad and Bax) induced apoptosis, regulated cyclin (including P53, P21, CDK4, CDK6, cyclin D3 and cyclin H) to inhibit cell cycle progression, and mediated epithelial-mesenchymal transition-like cell markers (including E-cadherin, N-cadherin, β-catenin, TCF-8, vimentin, Slug and Snail) to inhibit cell migration and invasion. In conclusion, the tumor-suppressor gene PTEN inhibited the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway and inhibited the proliferation and migration of Burkitt's lymphoma cells, induced apoptosis and cell cycle arrest, thus playing a crucial role in the pathogenesis of Burkitt's lymphoma.

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PTEN in kidney cancer: A review and meta-analysis

Cited by 39 publications

References 50 publications

<p>MiR-29b-3p Reverses Cisplatin Resistance by Targeting COL1A1 in Non-Small-Cell Lung Cancer A549/DDP Cells</p>

<p>MiR-29b-3p Reverses Cisplatin Resistance by Targeting COL1A1 in Non-Small-Cell Lung Cancer A549/DDP Cells</p>

Expression and clinical correlation of Survivin and PTEN in gastric cancer patients

Role and mechanism of PTEN in Burkitt's lymphoma

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