ArticleOncology letters2018
Shank-associated RH domain-interacting protein expression is upregulated in entodermal and mesodermal cancer or downregulated in ectodermal malignancy.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Central Facial Nervous System Biomolecules Involved in Peripheral Facial Nerve Injury Responses and Potential Therapeutic Strategies.Antioxidants (Basel, Switzerland) · 2023Review
- SHARPIN: Role in Finding NEMO and in Amyloid-Beta Clearance and Degradation (ABCD) Pathway in Alzheimer's Disease?Cellular and molecular neurobiology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Shank-associated RH domain-interacting protein (SHARPIN) is a type of linear ubiquitin chain-associated protein, which serves an important role in cell proliferation, apoptosis, organ development, immune and inflammatory reaction, initiation and development of malignant tumors. To evaluate SHARPIN expression in multiple malignant tumors derived from different germ layers, 14 types of cancer and their corresponding normal tissues were examined. Immunohistochemistry was performed to semi-quantify SHARPIN expression in multiple malignant tumors, and immunofluorescence was performed to evaluate the subcellular localization of SHARPIN in various malignant tumors. All the recruited cancer and paracancer samples originated from entoderm and mesoderm showed an upregulated expression of SHARPIN, whereas the cancer types that originated from ectoderm exhibited a downregulated or loss of SHARPIN expression. SHARPIN was primarily localized in the cytoplasm of cells and exhibited a faint signal in the nucleus, with the exception for lung cancer and esophagus cancer, in which malignant cells had aberrantly large nuclei and limited cytoplasm, which produced a signal in the nucleus but not in the cytoplasm. Conclusively, SHARPIN expression was upregulated in entodermal and mesodermal cancer types, but downregulated in ectodermal cancer types, indicating SHARPIN could act as either oncogene or anti-oncogene in malignant tumors derived from different germ layers.
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Registered trials
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