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All issues raised by the reviewers have been addressed. The manuscript is now ready for publication.
[# PeerJ Staff Note - this decision was reviewed and approved by Vladimir Uversky, a PeerJ Section Editor covering this Section #]
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The authors have successfully addressed the reviewers' comments. No further comments.
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• Title tightened and terminology standardized across the text (consistent use of “LINC01094”; LUSC vs. LSCC).
• Survey methodology expanded with explicit time window, databases searched, inclusion/exclusion logic, duplicate/retraction handling, and a selection flow with a summary table in the Supplement.
• Figure 2 now documents the database source/version and normalization, and the underlying numeric values are provided as supplementary data.
• Predicted miRNA partners are clearly labeled as predictions with tools/thresholds specified and distinguished from validated axes.
• The retracted ovarian-cancer citation has been removed and statements supported by valid sources.
• The description of miRNA mechanism is corrected to the canonical model (translational repression/mRNA destabilization).
• The PTEN/PI3K/AKT relationship is clarified in line with the literature (i.e., PTEN antagonizes PI3K/AKT; LINC01094 downregulation of PTEN activates PI3K/AKT).
The article fits the journal’s aims for a literature review. The narrative approach is acceptable
The central conclusion—that LINC01094 is frequently upregulated across cancers and functions mainly via ceRNA interactions with additional nucleus‑localized activities—is generally supported by primary literature. Representative examples include the SPI1/CCL7 axis driving macrophage accrual and dissemination in lung adenocarcinoma; AZGP1‑PTEN/AKT modulation in gastric cancer; and radioresistance in ccRCC via the miR‑577/CHEK2/FOXM1 pathway. These mechanistic claims are appropriately cautious and concordant with cited studies.
The revision satisfactorily addresses the major concerns from my previous review and the manuscript is now suitable for publication
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This Review summarizes the multiple cancer biology functions of LINC01094 and aims to inspire innovations in the management of human malignancies. The manuscript is well constructed and can be accepted for publication after resolving the following minor considerations.
1 . The regulatory mechanisms of LINC01094 in cancers have been listed as an important part of the manuscript, which should be included in the Abstract section.
2. There are some cacography and typographical mistakes in the manuscript, such as the word “inihibitory” listed in the sentence “For instance, Zhao et al. demonstrated an inihibitory...”. Additionally, the sentence “Furthermore, existing evidence has reflected a close correlation between LINC01094 dys-regulation and angiogenesis and inflammation in GC tissues…” listed in the part of 2.1 Gastric cancer (GC), reflected and dys-regulation should be changed into “revealed” and “dysregulation”, respectively, and "and angiogenesis and inflammation" should be changed into "and angiogenesis as well as inflammation".
3 . The title of “Cancers with high LINC01094 expression and their characteristics” is overstated.
4. The authors should update some references as appropriate to ensure the most up-to-date and relevant literature is being cited.
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This is an article with cross-disciplinary interest, with a fairly novel topic and with an adequate background (but rather vague) in the Introduction section. The English is acceptable, the literature references are relevant, and the figures and tables are informative. The structure is very good.
My suggestions to improve the paper:
1. In the Introduction section, please remove phrases that are too general (the first sentence) since they do not add to the article. Also, from a clinical perspective, your second sentence is quite exaggerated since the CRISPR/Cas9 gene-editing method is not a well-established cancer therapy. In my opinion, you should rewrite lines 59-67 and be more specific, and briefly refer to other cancer therapies (for example, chemotherapy is effective on rapidly dividing cells, immunotherapy harnesses the immune system, etc).
2. Please change "Clinical features" to "Clinicopathological features" in Table 1
3. The legend of Figure 1 should be more detailed.
4. Although English is generally good, a revision from a native speaker should be made to improve the paper.
Please provide more details on the methodology used for searching the lncRNASNP2 database.
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The manuscript is clearly organized, within the journal's scope, and the figures and tables support the narrative synthesis across tumor types. To strengthen clarity and transparency with minimal burden on the authors: (1) tighten the title to “Implications of LINC01094 for human malignancies” and standardize terminology throughout (use “LINC01094” consistently; use “LUSC” for lung squamous carcinoma and reserve “LSCC” for laryngeal squamous carcinoma—see the NSCLC section on p. 11 and “Other malignancies” on pp. 12–13); (2) expand the survey methodology with exact search dates, full query strings, and any language restrictions (pp. 8–9); and (3) for Figure 2, report the database source/version and retrieval date and share the underlying numeric values as a brief supplementary file.
The article fits the journal’s aims for a literature review. The narrative approach is acceptable, but the selection process should be more transparent to support comprehensive and unbiased coverage. Concretely: report the end date of the search, inclusion/exclusion criteria (e.g., human vs. cell/animal, discovery vs. validation cohorts), and how duplicates or retractions were handled. A simple flow description and a summary table of included primary studies with model systems and readouts (e.g., xenograft vs. in vitro only) would markedly increase utility without turning the work into a full systematic review. Because Figure 2 constitutes a new analysis/visualization based on an external database, please specify the exact resource and version (lncRNASNP2 and/or v3), normalization (RPKM/TPM), and tumor cohorts, and share the extracted data file. Also, where the manuscript proposes predicted targets of LINC01094 (miR‑139/195/200), indicate the tools and thresholds used or move these predictions to the Supplementary Methods.
The central conclusion—that LINC01094 is frequently upregulated across cancers and functions mainly via ceRNA interactions with additional nucleus‑localized activities—is generally supported by primary literature. Representative examples include the SPI1/CCL7 axis driving macrophage accrual and dissemination in lung adenocarcinoma; AZGP1‑PTEN/AKT modulation in gastric cancer; and radioresistance in ccRCC via the miR‑577/CHEK2/FOXM1 pathway. These mechanistic claims are appropriately cautious and concordant with cited studies. That said, two corrections are essential for factual accuracy. First, the ovarian cancer paper by Chen et al. (2021, Exp Ther Med), cited for Wnt/β‑catenin regulation, was retracted in 2024; statements that rely on this source should be qualified or removed and supported instead by the 2020 J Ovarian Research study or other valid evidence. Second, the description of miRNA action as causing “mRNA demethylation” is incorrect; canonical miRNA mechanisms involve translational repression and/or mRNA destabilization via 3′UTR binding, and ceRNA models rest on competition for shared miRNAs. Please revise those sentences and the related figure captions accordingly. Finally, in Figure 3, the legend currently reads as if PTEN were “activated” alongside PI3K/AKT; PTEN is the antagonist of PI3K/AKT, so the text should state that LINC01094 downregulates PTEN and thereby activates PI3K/AKT (consistent with the cited gastric study).
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