A newly published review in the journal Cell Division has brought together, for the first time, the scattered evidence on a long non-coding RNA called LINC01140 and its involvement in human cancers. The review, authored by Wen-Jing Men and Xiang-Sheng Wen and published on 5 July 2026, systematically surveys the expression patterns, functional roles and clinical significance of this molecule across multiple cancer types. Its central conclusion is striking: LINC01140 does not behave uniformly across the disease landscape. In some cancers it acts as an oncogene, driving proliferation, migration and invasion, while in others it functions as a tumor suppressor, restraining cell growth and spread. This duality, the authors argue, makes LINC01140 both a scientifically intriguing molecule and a candidate biomarker whose clinical use will require careful, cancer-type-specific validation.
Long non-coding RNAs are RNA molecules that are transcribed from the genome but are not translated into proteins. Far from being genetic noise, many of them have been shown to regulate gene expression, and accumulating evidence links them to disease, including cancer. Some lncRNAs promote tumor initiation and progression; others inhibit abnormal cell proliferation. LINC01140 is a recently identified member of this family, and the review’s starting observation is that it exhibits abnormal expression in cancerous tissues. The authors note that no previous review had systematically examined the relationship between LINC01140 expression and cancer, which motivated their comprehensive literature survey across pan-cancer.
The expression data compiled in the review reveal a markedly inconsistent picture across tissues. LINC01140 is overexpressed in gastric cancer, invasive bladder cancer and lung cancer tissues, whereas it is expressed at low levels in breast cancer tissues. The molecule also shows differential expression across cancer cell lines. In nasopharyngeal carcinoma cell lines including CNE2Z, S18-1C3 and CNE, LINC01140 expression was significantly reduced compared with the NP69 cell line. Relative to hFOB1.19 cells, expression was significantly elevated in the osteosarcoma cell lines Saos2 and MG63. In breast cancer cell lines HCC1937, MDA-MB-231 and MCF-7, LINC01140 levels were significantly lower than in the non-tumorigenic MCF-10A cell line.
Even within a single cancer type, the published findings conflict. In lung cancer, Xia and colleagues observed significant upregulation of LINC01140 in the A549, 95-D, NCI-H226, H1975, H292 and EBC-1 cell lines compared with BEAS-2B and HBE cells, whereas Wang and colleagues reported significant downregulation in A549 and H1299 cells relative to HBE cells. The review’s authors take these contradictions seriously and devote part of their analysis to explaining them. They point to heterogeneity among patient populations, including differences in racial background, tumor stage, smoking history and treatment history across studies. They also cite variation in detection methods: although quantitative reverse transcription PCR is widely used, differences in sensitivity, specificity and data normalization procedures, including the selection of reference genes and threshold settings, may affect the consistency of results. Molecular heterogeneity among cancer subtypes may further produce distinct expression patterns of LINC01140.
Functional experiments in cells reinforce the dual character of the molecule. In nasopharyngeal carcinoma cells (CNE2Z and S18-1C3), lung cancer cells (A549 and H1299) and breast cancer cells (MDA-MB-231, HCC1937 and MCF-7), LINC01140 suppresses proliferation and promotes apoptosis. It also inhibits colony formation in nasopharyngeal carcinoma cells and in MCF-7 and MDA-MB-231 breast cancer cells. In contrast, LINC01140 promotes proliferation in osteosarcoma cells (Saos2 and MG63), gastric cancer AGS cells, invasive bladder cancer T24 cells, and lung cancer A549 and EBC-1 cells, and it enhances the colony-forming ability of A549 and EBC-1 cells. In animal work, LINC01140 promoted the tumorigenic capacity of A549 lung cancer cells in nude mice while suppressing the tumorigenic capacity of MCF-7 and HCC1937 breast cancer cells in the same model system.
Metastasis-related behavior follows a similarly split pattern. LINC01140 promotes migration and invasion in osteosarcoma, gastric cancer AGS, invasive bladder cancer T24, and lung cancer A549 and EBC-1 cells. By contrast, it inhibits invasion in A549 and H1299 lung cancer cells and in MDA-MB-231 and MCF-7 breast cancer cells, and it suppresses migration in MDA-MB-231, HCC1937 and MCF-7 cells. The molecule also influences responses to therapy in cell models: it reduces the radiosensitivity of nasopharyngeal carcinoma cells. Here again the lung cancer literature diverges, with Xia and colleagues reporting that LINC01140 promoted cisplatin resistance in A549 and EBC-1 cells, while Wang and colleagues reported that it suppressed cisplatin resistance in A549 and H1299 cells. These are cell-line and animal-model findings, and the review does not claim therapeutic efficacy in patients.
Mechanistically, a central theme of the review is that LINC01140 acts as a molecular sponge for specific microRNAs, thereby regulating downstream target genes. The molecule can promote or inhibit the expression of target genes through interactions with miR-139-5p, miR-140-5p, miR-33a-5p, miR-33b-5p, miR-4742-5p, miR-200b-3p and miR-452-5p, and through these interactions it affects cancer cell growth and metastasis. Two worked examples illustrate the logic. Li and colleagues reported that LINC01140 suppresses the growth and metastasis of nasopharyngeal carcinoma and breast cancer by inhibiting miR-452-5p expression and subsequently promoting the expression of the ZNF621 and RGS2 genes. Singh and colleagues reported the opposite direction of effect in different cancers: LINC01140 promotes the growth and metastasis of gastric cancer and bladder cancer by enhancing miR-140-5p expression and thereby suppressing FGF9 gene expression. In gastric cancer cells specifically, inhibition of LINC01140 impedes proliferation, migration and invasion through the miR-140-5p/FGF9 signaling axis.
The review also documents cases in which LINC01140 regulates target genes directly rather than through microRNAs. In osteosarcoma cells, inhibiting LINC01140 suppresses growth and metastasis by inhibiting epithelial-mesenchymal transition characteristics. In gastric cancer AGS and bladder cancer T24 cells, survival and metastatic capacity can be suppressed through inhibition of Ki-67, MMP-2 and MMP-9 expression. In breast cancer cells, overexpression of LINC01140 suppresses the protein expression of Bcl-2, beta-catenin, C-myc and Wnt within the Wnt/beta-catenin signaling pathway while increasing the protein levels of Bax and p-GSK-3 within the same pathway, thereby inhibiting breast cancer cell proliferation. Whether LINC01140 possesses direct regulatory functions independent of the competing endogenous RNA network remains, according to the authors, an open question for future research.
On the clinical side, the review finds that aberrant LINC01140 expression is significantly associated with patient survival, clinical stage and disease diagnosis, although the specific associations differ by cancer type. Overexpression of LINC01140 is significantly associated with overall survival, diagnostic value, pathological stage, T stage, N stage and tumor differentiation in patients with gastric cancer. Overexpression is also significantly associated with overall survival, pathological stage and metastasis in patients with lung cancer. In breast cancer, it is low expression of LINC01140 that is significantly associated with diagnostic value. The authors present these associations as evidence that LINC01140 has the potential to serve as a biomarker for cancer diagnosis and prognosis, while stressing that the currently available sample size remains relatively limited and that additional clinical samples are required to validate the expression patterns and biological functions of the molecule.
Looking forward, the review identifies several priorities. The mechanisms underlying the opposing functions of LINC01140 in different cancer types require further clarification. The reliability and specificity of the molecule as a diagnostic and prognostic biomarker need validation in large clinical cohorts, together with evaluation of its potential application as a non-invasive liquid biopsy biomarker. The authors also flag the development of targeted therapeutic strategies against LINC01140, including antisense oligonucleotides and small-molecule inhibitors, as a long-term objective that may be particularly valuable in cancer types that depend on the oncogenic functions of the molecule. For now, the review’s contribution is consolidation: a single, organized account of what is known about an RNA whose behavior flips between oncogene and tumor suppressor depending on the cancer in which it is measured, and a reminder that biomarker candidates emerging from cell and animal studies must clear substantial clinical hurdles before they reach practice.
Subject of Research: The dual oncogenic and tumor-suppressive roles of the long non-coding RNA LINC01140 across human cancers
Article Title: The roles and clinical significance of LINC01140 in human cancers in the real world
Article References: Men, W.-J., & Wen, X.-S. (2026). The roles and clinical significance of LINC01140 in human cancers in the real world. Cell Division, 21(1), Article 19. https://doi.org/10.1186/s13008-026-00191-3
Image Credits: AI Generated
DOI: 10.1186/s13008-026-00191-3
Keywords: LINC01140, long non-coding RNA, cancer biomarker, gastric cancer, breast cancer, lung cancer, nasopharyngeal carcinoma, osteosarcoma, bladder cancer, miRNA, Wnt/beta-catenin signaling, prognosis
News Source: Nathaniel Bowman. (October 28, 2026). Long Non-Coding RNA LINC01140 Shows Dual Roles Across Human Cancers, Review Finds. Scienmag.
