ArticleThe Kaohsiung journal of medical sciences2026
The Regulatory Role and Mechanism of Myoferlin in Mitophagy During Papillary Thyroid Carcinogenesis.
Article in The Kaohsiung journal of medical sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Papillary thyroid carcinoma (PTC) is the most prevalent subtype of thyroid cancer; however, the regulatory mechanisms by which mitophagy influences its progression remain inadequately elucidated. This study sought to examine the role of myoferlin (MYOF) in mitophagy and its molecular basis during PTC development. Utilizing three paired PTC and adjacent normal tissues, we observed elevated MYOF expression at both protein and mRNA levels through western blot and qRT-PCR analyses. Stable MYOF knockdown cell lines were established in PTC (TPC-1, KTC-1) and normal thyroid (Nthy-ori 3-1) cells using lentiviral shRNA. Functional assays, including CCK-8, wound healing, transwell, flow cytometry, immunofluorescence, and mitophagic flux analysis, along with a xenograft mouse model, were employed. Subsequent evaluations involved hematoxylin and eosin staining, immunohistochemistry, western blot, and qRT-PCR. As a result, MYOF was significantly upregulated in PTC tissues and TPC-1 cells. Knockdown of MYOF inhibited PTC cell proliferation, invasion, migration, and colony formation, while promoting apoptosis. Mechanistically, MYOF was found to regulate PTC progression through the PINK1/Parkin-mediated mitophagy pathway. In vivo xenograft experiments demonstrated that MYOF silencing suppressed tumor growth and increased the expression of mitophagy-related proteins BNIP3 and NIX. In conclusion, MYOF drives PTC progression by repressing mitophagy. Targeted inhibition of MYOF activates tumor-suppressive mitophagy via the PINK1-Parkin axis, indicating MYOF as a potential therapeutic target in PTC.
Indexed as
Identifiers
What OpenQuestion holds
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.