Cancer is one of the most prevalent and deadly diseases, ranking first or second among noncommunicable diseases in terms of morbidity and mortality [1, 2]. Despite significant advances in cancer therapy over the past several decades, the survival rate, especially for those with advanced cancer and metastasis, remains poor [2].

Therefore, developing more effective clinical strategies and gaining a deeper understanding of the molecular mechanisms driving tumor growth are imperative [3, 4]. Among them, recent studies have highlighted that noncoding RNAs could be pivotal players in cancer pathogenesis [5]. Advances in epigenetic engineering,

such as zinc finger–based control of immune genes, show how targeted gene regulation can be used therapeutically. Similar mechanisms of transcriptional and epigenetic modulation are also central to the oncogenic functions of lncRNAs like MSC-AS1 [6].

lncRNAs, which are RNA molecules longer than 200 nucleotides, have been found to play a crucial role in regulating various biological processes, including growth, chromatin dynamics, differentiation, progression, and gene expression [7, 8]. Unlike mRNAs, lncRNAs lack protein-coding capacity [9]. However, recent research using innovative molecular approaches has revealed the presence of small open reading frames (sORFs) in some lncRNAs, enabling them to interact with ribosomes and encode short peptides [10, 11]. Numerous investigations have demonstrated that lncRNAs function as principal regulators of the treatment response, onset, and tumor progression in cancer [12, 13]. For instance, lncRNA MALAT1 suppresses metastasis and shows an inverse correlation with breast cancer progression, underscoring its potential as a metastasis-inhibiting lncRNA [14]. Moreover, research revealed that the HOXB-AS3-encoded peptide inhibits colorectal cancer (CRC) development, and loss of this peptide is correlated with a worse prognosis for CRC [15]. MSC-AS1, a novel lncRNA molecule, has recently emerged as an important factor in tumor development [16-19]. A study found that MSC- AS1 overexpression promotes the development of liver cancer by increasing the expression of Phosphoglycerate Kinase 1 (PGK1) [20]. Another study revealed that MSC-AS1 regulates the miR-524-5p/NR4A2 axis, thereby promoting nasopharyngeal carcinoma [21]. Additionally, MSC-AS1 may enhance the differentiation of bone marrow mesenchymal stem cells (BMSCs) into osteoblasts [22]. It has also been shown to aggravate nasopharyngeal carcinoma by sponging miR-524-5p, leading to increased NR4A2 expression [21]. Furthermore, Hu et al. demonstrated that MSC-AS1 regulates the migration and proliferation of kidney renal clear cell carcinoma (KIRC) cells through the miR-3924/WNT5A/ β-catenin axis [23].

This review aims to provide an in-depth overview of recent findings on the abnormal expression, molecular mechanisms, and clinical relevance of MSC-AS1 in various cancers.

This review aims to provide a comprehensive overview of the role of MSC-AS1 in various human cancers. To ensure broad coverage and minimize selection bias, no restrictions were applied regarding cancer type, experimental model, or publication date. A thorough search of the scientific literature was conducted using well-established databases, including PubMed, Scopus, Web of Science, and Google Scholar. The search strategy employed a combination of keywords such as “MSC-AS1,” “long non-coding RNA,” “cancer,” “tumor progression,” “prognostic biomarker,” “chemoresistance,” and “lncRNA–miRNA–mRNA axis.” Studies published up to May 20, 2024, were considered. Only peer-reviewed articles written in English and focusing on the biological functions, molecular mechanisms, diagnostic and prognostic relevance, and therapeutic potential of MSC-AS1 were included in this review.

RNA polymerase II (Pol II) is responsible for the transcription of lncRNAs, which are characterized by the addition of a 5′ methyl-cytosine cap and 3′ poly (A) tail [24]. These molecules can be classified based on their genetic origin into long intergenic, intronic, and exonic lncRNA, and based on transcriptional orientation as sense or anti-sense lncRNA. Additionally, they can be classified into macro and retained intron lncRNAs based on splicing-based classification [25]. LncRNAs are crucial in numerous physiological and pathological processes by either activating or suppressing gene expression [26]. Primarily, they function as transcriptional regulators through interactions with transcriptional complexes, chromatin remodeling, or by serving as scaffolds that recruit various molecules [27]. Moreover, lncRNAs regulate the expression of genes by interacting with DNA, RNA, and protein near enhancers or promoters of target genes [28]. These interactions occur via a variety of methods, such as guide, scaffold, decoy, and signal [26]. Enzymatically or regulatory active protein complexes are bound by guide lncRNAs, which then direct the complexes to specific target gene promoters or chromosomal areas to regulate downstream signaling pathways and expression of genes [8]. Moreover, lncRNAs may be related to pancreatic cancer (PC) via regulating various post-transcriptional protein molecules, promoting or suppressing gene transcription, or interacting with miRNA to regulate or increase its expression. In this manner, lncRNAs can act as regulators for cancer suppressors or proto-oncogene genes [29] (Figure 1 and 2).

There is no doubt that cancer is a life-threatening disease that poses a major risk to human health. Since the coding genome accounts for less than 2 percent of all gene sequences, most cancer phenotypes are driven by mutations in non-coding regions [30]. lncRNAs have been demonstrated to have a significant effect on various cellular processes, including angiogenesis, differentiation, migration, and proliferation [31, 32]. Aberrant lncRNA expression is common in cancer and can act as factors that either promote or inhibit tumor growth. In oral cancers, for example, the lncRNA ELDR is overexpressed and activates the ILF3-cyclin E1 axis signaling. ELDR suppression markedly reduces the growth of oral cancer cells [33]. In colorectal cancer, it has been discovered that the lncRNA ZFAS1 stimulates tumor growth and metastasis while inhibiting apoptosis. Additionally, studies have indicated that ZFAS1 overexpression is associated with poor prognosis in patients with colorectal cancer [34]. LINC00460 has been shown to promote the growth of cervical cancer cells and suppress apoptosis by downregulating miRNA-503-5p to advance cervical cancer progression. LINC00511 has been shown to upregulate MMP-13 and decrease miRNA-150 expression, driving invasion and proliferation [35, 36]. Conversely, lncRNA TUSC7 has been shown to sponge miRNA-23b to suppress epithelial-mesenchymal transition ( EMT) and metastasis in CRC. TSLC8 lncRNA has also been shown to increase stability, leading to reduced colony formation and survival of CRC. Collectively, these findings indicate that lncRNAs have a bright future as cancer therapeutic targets [37-39].

MSC-AS1 is classified as an lncRNA that does not code for proteins but performs other cellular functions. It has been associated with several types of cancer, including laryngeal cancer, colorectal cancer, and gastric cancer. MSC-AS1 may also influence the ability of mesenchymal stem cells to differentiate into various tissues, such as bone, cartilage, and fat. Evidence suggests that MSC-AS1 affects cancer progression and stem cell function by modulating the expression of genes involved in the PI3K/Akt pathway, which is essential for cell survival, proliferation, and division (Figure 1). MSC-AS1 is classified as a long non-coding RNA (lncRNA) that does not code for proteins but performs other cellular functions. It has been associated with several types of cancer, including laryngeal cancer, colorectal cancer, and gastric cancer. MSC-AS1 may also influence the ability of mesenchymal stem cells to differentiate into various tissues, such as bone, cartilage, and fat. Evidence suggests that MSC-AS1 affects cancer progression and stem cell function by modulating the expression of genes involved in the PI3K/Akt pathway, which is essential for cell survival, proliferation, and division (Figure 1).

Glioma is a prevalent kind of brain cancer, making up around 40-50% of tumors that occur inside the skull [66]. Despite advancements in medical treatment techniques, the median survival duration for patients with glioma remains below one year [67]. ncRNAs play a crucial role in the progression and development of Glioma. Significantly, lncRNAs and microRNAs have particular relevance among them [68].

Li et al. found that MSC-AS1 expression was elevated in glioma tissues and cells that exhibited resistance to temozolomide (TMZ). Suppression of MSC-AS1 led to decreased resistance to TMZ and increased cell death. The influence of miR-373-3p was found to be reversible by silencing this microRNA, which directly targeted CPEB4 and affected the PI3K/Akt signaling pathway. Furthermore, knocking down miR-373-3p reversed the effects of CPEB4 or MSC-AS1 suppression on TMZ sensitivity. The study indicated that the PI3K/Akt pathway regulates the miR-373-3p/CPEB4 axis through MSC-AS1 knockdown, ultimately inhibiting the growth of TMZ- resistant glioma cells. Overall, MSC-AS1 inhibition suppressed glioma growth and enhanced TMZ sensitivity both in vitro and in vivo, highlighting its potential as a therapeutic target [47].

Melanoma is one of the most aggressive and lethal forms of skin cancer, and its incidence and mortality rates continue to rise despite considerable preventive efforts [69]. Early detection and treatment of melanoma might somewhat decrease the occurrence rate [70]. ncRNAs have significant involvement in the development and advancement of melanoma. Notably, lncRNAs and microRNAs have special importance among them.

Ma et al. demonstrated that the expression levels of MSC-AS1 and lymphoid enhancer-binding factor 1 (LEF1) were elevated in melanoma cell lines, while the expression of microRNA 302a-3p (miR-302a-3p) was reduced. Their study revealed that silencing MSC-AS1 inhibited migration, cell proliferation, and EMT in vitro, as well as tumor growth in vivo. Additionally, MSC-AS1 was found to modulate LEF1 expression by functioning as a sponge that recruits insulin-like growth factor 2 mRNA- binding protein 2 (IGF2BP2) and miR-302a-3p. The tumor progression rescue facilitated by the overexpression of LEF1 was hindered by the knockdown of MSC-AS1. Collectively, these findings indicate that the MSC-AS1/ miR-302a-3p/IGF2BP2/LEF1 axis plays a crucial role in melanoma progression and that MSC-AS1 may represent a promising biomarker and therapeutic target in melanoma [48].

Osteosarcoma (OS) is the most common primary malignant bone tumor, characterized by multiple genetic abnormalities and the uncontrolled proliferation of mesenchymal cells that produce immature bone or malignant osteoid [71, 72]. ncRNAs play a crucial role in the progression and development of OS. Significantly, lncRNAs and microRNAs have particular relevance among them.

Zhang et al. demonstrated that silencing MSC-AS1 led to decreased proliferation, invasion, and migration of OS cells, while increasing apoptosis. Additionally, the suppression of MSC-AS1 heightened the susceptibility of OS cells to cisplatin (DDP). Their findings indicated that MSC-AS1 knockdown resulted in reduced levels of CDK6 and miR-142 expression, which subsequently decreased the protein expression of pPI3K/t-PI3K and pAKT/t-AKT. Furthermore, the suppression of MSC-AS1 impeded the progression of osteosarcoma in vivo by enhancing miR-142 levels, lowering CDK6 expression, and inactivating the PI3K/AKT signaling pathway. these findings highlight MSC-AS1 as a potential therapeutic target and suggest novel treatment strategies for osteosarcoma [19].

Early cancer detection is critical for effective treatment, yet current diagnostic methods often lack the specificity and sensitivity required for reliable early-stage identification [73]. This highlights the need for novel biomarkers that can improve early diagnosis and prognosis. Recent investigations have identified MSC-AS1 as a promising diagnostic and prognostic biomarker across several cancer types [41]. ncRNAs play a crucial role in the progression and development of hepatocellular carcinoma (HCC). Significantly, lncRNAs and microRNAs have particular relevance among them. MSC-AS1 is elevated in PDAC tissues, associated with a worse prognosis. Silencing of MSC-AS1 suppresses cell proliferation, but the elevated expression of miR-29b-3p is associated with improved prognosis. In gastric cancer, increased MSC-AS1 levels are substantially correlated with T stage, histological type, and grade, TP53 status, and PIK3CA status. Elevated MSC-AS1 expression forecasts reduced overall survival and progression-free interval, with its independent association with overall survival validated by multivariate analysis. Zhang et al. discovered that MSC-AS1 lncRNA is markedly elevated in OS tissues relative to surrounding normal bone tissues and correlates with worse prognosis. Increased MSC-AS1 levels were detected in osteosarcoma cell lines relative to normal osteoblasts. Likewise, MSC-AS1 levels are elevated in NPC tissues, with heightened levels associated with advanced tumor grade and worse prognosis.

SUN et al. found that MSC-AS1 expression was increased in pancreatic ductal adenocarcinoma (PDAC) tissues. Elevated MSC-AS1 levels were linked to worse prognosis in PDAC patients. Silencing MSC-AS1 in Panc-1 and BxPC-3 cells led to a significant reduction in cell proliferation. Furthermore, miR-29b-3p, which is known for its tumor-suppressing role, was predicted to bind to both MSC-AS1 and CDK14. Unlike MSC-AS1, elevated levels of miR-29b-3p were correlated with improved prognosis in patients with PDAC [16]. A different study revealed that MSC-AS1 expression was significantly elevated in GC tissues compared to non-tumor tissues. Additionally, higher MSC-AS1 levels were observed in GC cell lines relative to normal gastric mucosal GES-1 cells. Data from The Cancer Genome Atlas (TCGA) also indicated that elevated MSC-AS1 expression is strongly associated with advanced poor prognosis and tumor stages in GC patients [42].

Another study showed that MSC-AS1 levels were higher in gastric cancer. They showed that a significant association between elevated MSC-AS1 expression and factors such as histological classification, histological grade, T stage, and the status of TP53 and PIK3CA. Moreover, they revealed that patients with high MSC- AS1 expression had worse overall survival and shorter progression-free intervals. Additionally, multivariate survival analysis confirmed that MSC-AS1 expression independently predicted overall survival [41].

Zhang et al. revealed that MSC-AS1 lncRNA levels were significantly higher in OS tissues than in the surrounding normal tissues. The analysis suggested that increased MSC-AS1 expression correlated with worse prognosis in OS patients [19]. Likewise, in nasopharyngeal carcinoma (NPC), elevated MSC-AS1 expression is associated with advanced tumor grade and poor prognosis. Collectively, these findings support the role of MSC-AS1 as a clinically relevant biomarker for cancer diagnosis and prognosis across multiple tumor types.

Chemotherapy remains one of the most widely used and effective treatment strategies for various cancers; however, its efficacy is often limited by the emergence of drug resistance. Although the mechanisms underlying this resistance are not fully understood, alterations within the tumor microenvironment (TME) are considered major contributors [74]. MSC-AS1 has been found to enhance chemotherapy resistance in various types of cancer, including glioma. In particular, MSC-AS1 levels are elevated in temozolomide (TMZ)-resistant cells and tissues. Patients with high MSC-AS1 expression tend to have shorter overall survival. Furthermore, reducing MSC-AS1 via knockdown impairs cell viability, proliferation, and sensitivity to TMZ in resistant glioma cells [47].

In gastric cancer, MSC-AS1 promotes cell proliferation and inflammatory mediator secretion while enhancing cisplatin resistance through the miR-142-5p/DDX5 axis [43]. MSC-AS1 interacts with miRNAs like miR-142-5p, miR-373-3p, and miR-425-5p to regulate chemotherapy resistance genes [45, 47]. MSC-AS1 promotes fatty acid oxidation (FAO) and stemness in gastric cancer cells, contributing to 5-FU and oxaliplatin resistance. MSC-AS1 influences cell cycle progression, apoptosis, and expression of proliferation markers like PCNA and Ki-67 to modulate chemosensitivity [45]. Collectively, these findings identify MSC-AS1 as a critical regulator of chemotherapy resistance in diverse cancers. Targeting MSC-AS1 and its downstream signaling pathways may provide a promising strategy to overcome resistance and improve the effectiveness of chemotherapeutic agents.

In conclusion, cancer research continues to evolve with emphasis on targeted therapies, epigenetic mechanisms, and environmental influences on tumor development across various types like ovarian, oral, and hepatocellular cancers. Biosensing advancements and regulatory networks further aid in diagnosis and treatment, highlighting nanotechnology’s broad potential in combating cancer [75-95]. lncRNAs are increasingly recognized as key regulators of tumor development, and MSC-AS1 has consistently demonstrated a strong association with tumor aggressiveness across multiple cancer types. Elevated MSC-AS1 expression correlates with adverse clinical features, including higher histological grade, larger tumor size, and reduced overall survival. Functional studies further support its oncogenic potential, showing that silencing MSC-AS1 significantly impairs cancer cell proliferation, invasion, and metastasis both in vitro and in vivo. These findings highlight MSC-AS1 as a promising candidate for prognostic biomarker development and therapeutic intervention. Although initial studies suggest its potential for early cancer detection, current evidence is insufficient for clinical application. Further validation through large-scale clinical trials and mechanistic studies is required to fully elucidate its diagnostic value, therapeutic feasibility, and underlying molecular pathways. Future investigations of MSC-AS1 may not only clarify lncRNA- driven mechanisms in tumorigenesis but also facilitate the development of innovative RNA-based biomarkers and precision therapies tailored to specific cancer subtypes.

Conflicts of Interest

The authors state that they have no competing interests or financial relationships relevant to this work.

Declaration

This manuscript was prepared without the use of any artificial intelligence (AI) tools or technologies.

Funding

Not applicable

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