ArticleCancer biotherapy & radiopharmaceuticals2015
Tumor protein D52-like 2 contributes to proliferation of breast cancer cells.
Article in Cancer biotherapy & radiopharmaceuticals, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- SMARCC2 combined with c‑Myc inhibits the migration and invasion of glioma cells via modulation of the Wnt/β‑catenin signaling pathway.Molecular medicine reports · 2021Article
- Tumor protein D52 promotes breast cancer proliferation and migration via the long non-coding RNA NEAT1/microRNA-218-5p axis.Annals of translational medicine · 2021Article
- Knockdown of lncRNAOncoTargets and therapy · 2020Article
- Increased expression of tumor protein D54 is associated with clinical progression and poor prognosis in patients with prostate cancer.Oncology letters · 2017Article
- Evaluation of autoantibody signatures in meningioma patients using human proteome arrays.Oncotarget · 2017Article
- Tumor Protein D52 (TPD52) Inhibits Growth and Metastasis in Renal Cell Carcinoma Cells Through the PI3K/Akt Signaling Pathway.Oncology research · 2017Article
- A tumor-suppressive microRNA, miRNA-485-5p, inhibits glioma cell proliferation and invasion by down-regulating TPD52L2.American journal of translational research · 2017Article
- Characterization of fusion genes and the significantly expressed fusion isoforms in breast cancer by hybrid sequencing.Nucleic acids research · 2015Article
Corrections and comments
- Correction · 2018-10-18Error in Text ·
- Retraction · 2017-12-01Concerns/Issues about Data · Concerns/Issues about Image · Investigation by Third Party · Objections by Third Party ·
- Retracted
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer is a major cause of cancer-related death among women. Tumor protein D52-like 2 (TPD52L2) is one member of the TPD52 family, which has been shown to function in mediating cell proliferation, apoptosis, and vehicle trafficking. TPD52 was originally identified in human breast carcinoma. In this study, the authors found that TPD52L2 is extensively expressed in multiple human breast cancer cell lines. To elucidate the functional role of TPD52L2 in breast cancer, the authors employed lentivirus-mediated short hairpin RNA (shRNA) to knock down TPD52L2 in one breast cancer cell line, ZR-75-30, which showed high TPD52L2 expression. The shRNA-mediated TPD52L2 knockdown inhibited the proliferation and colony formation in ZR-75-30 cells, as determined by MTT and colony formation assays. Knockdown of TPD52L2 led to an accumulation of cells in the G0/G1 phase of the cell cycle. Furthermore, knockdown of TPD52L2 promoted GSK3β phosphorylation in ZR-75-30 cells. This investigation indicates that TPD52L2 plays an essential role in the growth of breast cancer cells, which may contribute to provide gene therapy for breast cancer treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.