# N7-methyladenosine-induced SLC7A7 serves as a prognostic biomarker in pan-cancer and promotes CRC progression in colorectal cancer

Researcher: Ge Zhang
Chinese name: 张格
ORCID identity anchor: https://orcid.org/0000-0002-3116-3246
Canonical researcher: https://drgezhang.com/#person

Journal: Scientific Reports
Year: 2024
Type: Article
DOI: 10.1038/s41598-024-80885-2
Canonical page: https://drgezhang.com/papers/doi-10-1038-s41598-024-80885-2.html
Markdown record: https://drgezhang.com/papers/doi-10-1038-s41598-024-80885-2.md

## Full Authors

1. Fuqi Wang
2. Shiqian Zhang
3. Zhuang Chen
4. Xiaoming Gu
5. Ge Zhang
6. Hairong Zhang
7. Weitang Yuan

## About this record

This is an author-controlled publication record in the Ge Zhang Academic Hub. It identifies this work as part of Ge Zhang’s publication record via ORCID; the publisher version remains the version of record.

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## Research context and source limits

Limited evidence note. Only the source material identified below has been reviewed; this is not a complete Paper GEO V2 assessment.

Separately verified cell-assay observations; RNA-modification identity and full mechanistic interpretation are unresolved.

### Research question and experimental setting

The paper combines cancer-expression analyses with colorectal-cancer cell experiments involving SLC7A7. The inspected assays use HCT116 and SW480 cells, with RNA interference and measurements of migration, invasion and molecular expression. These are experimental cell-model observations, not evidence that targeting SLC7A7 benefits patients.

Source: [Methods: Cell culture; RNA interference; cell migration/invasion methods; Figure 5A–E](https://www.nature.com/articles/s41598-024-80885-2)

### What the inspected figures support

Figure 5A–E reports reduced migration and invasion after SLC7A7 knockdown in the two cell lines. Figure 6C identifies APC as the measured analyte and shows increased APC expression after knockdown. These limited observations can be distinguished from the paper’s broader RNA-modification mechanism; no animal sample size is inferred from displayed examples.

Source: [Figure 5A–E; Figure 6C; Animal models and Figure 5F](https://www.nature.com/articles/s41598-024-80885-2)

### Unresolved molecular identity

The official title says N7-methyladenosine, whereas the abstract and mechanistic assays refer to N7-methylguanosine/m7G. A complete mechanism-centred V2 cannot silently choose or rename the modification. This disclosure preserves the formal title while withholding endorsement of the disputed mechanistic identity.

Source: [Title versus Abstract; mechanistic Results; Figure 6E–I; Supplementary Figure 4](https://www.nature.com/articles/s41598-024-80885-2)

### Evidence limits

- Cell-model results do not establish clinical treatment efficacy.
- Modification identity and animal replicate accounting still require clarification.

### Provenance

- [Article source](https://www.nature.com/articles/s41598-024-80885-2) — Official publisher or PMC full text reviewed locally. Methods: Cell culture; RNA interference; cell migration/invasion methods; Figure 5A–E

Source review: 2026-10-27.

## Cite this paper

Fuqi Wang, Shiqian Zhang, Zhuang Chen, Xiaoming Gu, Ge Zhang, Hairong Zhang, Weitang Yuan. N7-methyladenosine-induced SLC7A7 serves as a prognostic biomarker in pan-cancer and promotes CRC progression in colorectal cancer. Scientific Reports. 2024. https://doi.org/10.1038/s41598-024-80885-2

- [BibTeX](https://drgezhang.com/citations/doi-10-1038-s41598-024-80885-2.bib)
- [RIS / EndNote](https://drgezhang.com/citations/doi-10-1038-s41598-024-80885-2.ris)
- [CSL JSON](https://drgezhang.com/citations/doi-10-1038-s41598-024-80885-2.csl.json)

## Links

- DOI: https://doi.org/10.1038/s41598-024-80885-2
- HTML page: https://drgezhang.com/papers/doi-10-1038-s41598-024-80885-2.html
- Google Scholar query: https://scholar.google.com/scholar?q=%22N7-methyladenosine-induced%20SLC7A7%20serves%20as%20a%20prognostic%20biomarker%20in%20pan-cancer%20and%20promotes%20CRC%20progression%20in%20colorectal%20cancer%22
- ORCID: https://orcid.org/0000-0002-3116-3246