Evidence map›Paper›PMID 41088065›Full record

ArticleBMC cancer2025

SLIT2 modulates NMIIA to regulate mitophagy and suppress hepatocellular carcinoma progression.

Yong Qin, Junbin Zhou, Shimiao Li, Xiaofeng Liu, Shengqian Xu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Yong QinDepartment of Hepatobiliary Pancreatic Surgery, Lishui Hospital of Wenzhou Medical University, The First Affiliated Hospital of Lishui University. Lishui People's Hospital, East of the intersection of National Highway 330 and Liyang Street, Liandu district, Lishui, Zhejiang, 323000, China.
Junbin ZhouDepartment of Hepatobiliary Pancreatic Surgery, Lishui Hospital of Wenzhou Medical University, The First Affiliated Hospital of Lishui University. Lishui People's Hospital, East of the intersection of National Highway 330 and Liyang Street, Liandu district, Lishui, Zhejiang, 323000, China.
Shimiao LiDepartment of Hepatobiliary Pancreatic Surgery, Lishui Hospital of Wenzhou Medical University, The First Affiliated Hospital of Lishui University. Lishui People's Hospital, East of the intersection of National Highway 330 and Liyang Street, Liandu district, Lishui, Zhejiang, 323000, China.
Xiaofeng LiuDepartment of Hepatobiliary Pancreatic Surgery, Lishui Hospital of Wenzhou Medical University, The First Affiliated Hospital of Lishui University. Lishui People's Hospital, East of the intersection of National Highway 330 and Liyang Street, Liandu district, Lishui, Zhejiang, 323000, China.
Shengqian XuDepartment of Hepatobiliary Pancreatic Surgery, Lishui Hospital of Wenzhou Medical University, The First Affiliated Hospital of Lishui University. Lishui People's Hospital, East of the intersection of National Highway 330 and Liyang Street, Liandu district, Lishui, Zhejiang, 323000, China. lsxsq123@163.com.

Funding

Lishui City self-funded public welfare technology application research project No. 2022SJZC030Zhejiang basic public welfare research project No. LGF22H160059
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is characterized by aggressive progression and metastasis, driven by complex molecular interactions. This study elucidates the functional roles of slit guidance ligand 2 (SLIT2) and non-muscle myosin IIA (NMIIA) in HCC and explores their mechanistic interplay. Immunofluorescence and quantitative PCR (Q-PCR) analyses demonstrated significant downregulation of SLIT2 and upregulation of NMIIA in HCC tissues, with SLIT2 expression inversely correlating with tumor stage and metastatic propensity, as validated by The Cancer Genome Atlas (TCGA) dataset. Functional assays revealed that SLIT2 overexpression attenuated HCC cell proliferation, migration, and invasion, whereas NMIIA overexpression markedly enhanced these oncogenic properties. Mechanistically, NMIIA facilitated epithelial-mesenchymal transition (EMT) and mitophagy, potentiating tumor progression. Conversely, SLIT2 overexpression inhibited myosin regulatory light chain (MRLC) phosphorylation, thereby suppressing NMIIA activity, EMT, and mitophagy. SLIT2 also diminished cell adhesion, while NMIIA enhanced adhesion and colony-forming capacity. In vivo xenograft studies corroborated that SLIT2 depletion accelerated tumor growth. These findings establish the SLIT2/NMIIA axis as a critical modulator of HCC progression and a promising therapeutic target.

Indexed as

Carcinoma, HepatocellularIntercellular Signaling Peptides and ProteinsLiver NeoplasmsMitophagyNerve Tissue ProteinsAnimalsCell Line, TumorCell MovementCell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeIntercellular Signaling Peptides and ProteinsNerve Tissue ProteinsSlit Homolog 2 ProteinEpithelial-mesenchymal transitionHepatocellular carcinomaMitophagyNon-muscle myosin IIASlit guidance ligand 2

Identifiers

PMID41088065
PMCPMC12519854

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.