Long non-coding RNAs (lncRNAs) have emerged as pivotal regulators in the complex landscape of cellular biology, gaining significant prominence in cancer research [1,2,3,4]. These RNA molecules, exceeding 200 nucleotides and lacking protein-coding capacity [5, 6], were once dismissed as “junk RNAs” [7, 8]. However, the rapid advancement of high-throughput sequencing technologies, such as RNA-Seq and single-cell sequencing techniques, along with progress in bioinformatics in recent years, have led to the identification of an increasing number of lncRNAs [9,10,11,12,13,14]. Many of these lncRNAs are now known to play vital roles in various physiological processes [15,16,17,18,19]. For example, HOTAIR, one of the earliest reported lncRNAs [20, 21], has been recognized as a significant oncogenic driver [22,23,24,25], contributing to tumor cellular signaling transduction [26,27,28], cancer metabolism reprogramming [29,30,31,32], and tumor metastasis [33,34,35,36]. Another notable lncRNA, H19, is known for its involvement in embryonic development and imprinting regulation [37,38,39,40,41,42].

LncRNAs exhibit diverse functions by participating in various cellular processes, such as cell proliferation [43,44,45], cellular metabolism [46,47,48], and cellular senescence [49, 50]. And lncRNAs often exhibit dysregulation and are implicated in a range of diseases [51,52,53,54,55], including atherosclerosis [56,57,58], Alzheimer’s disease [59,60,61], rheumatoid arthritis [62,63,64], and particularly in human tumors [65,66,67,68,69,70]. Notably, lncRNA has emerged as the promising target for the treatment of human diseases [71,72,73]. Especially with the development of CRISPR/Cas9 technology, lncRNA genes can be precisely manipulated to study their role in disease [74,75,76,77]. This helps identify new lncRNAs that are expected to become new targets and biomarkers for cancer treatment. Furthermore, the use of CRISPR/Cas9-based screens to discover lncRNAs involved in drug resistance also opens avenues for the development of more effective therapeutic strategies [78]. These advances underscore the importance of lncRNA in precision medicine and cancer treatment and mark an important step forward for customized medical solutions.

LncRNAs are broadly categorized into several types based on their genomic locations, encompassing intronic, intergenic, and antisense lncRNAs [79,80,81,82]. LncRNAs play crucial roles in regulating gene expression at multiple levels, including chromatin modification, transcription, and post-transcriptional processing [83,84,85,86,87,88]. Among these, antisense lncRNAs have recently garnered attention since their critical role in the tumor development [89, 90]. Antisense lncRNAs are types of long noncoding RNA molecules that are transcribed from the DNA strand opposite to the sense strand [91]. These RNAs can regulate gene expression through various mechanisms [89, 90, 92], including base pairing with sense RNAs, affecting their stability, translation, and splicing, or by recruiting chromatin-modifying enzymes to specific genomic regions. Their actions contribute to complex regulatory networks within cells, influencing numerous biological processes and disease states.

SLC16A1 antisense RNA 1 (SLC16A1-AS1) is a novel antisense lncRNA which has become a rising star in oncological research. SLC16A1-AS1 exhibits aberrant expression in a variety of cancers, including glioblastoma (GBM) [93, 94], oral squamous cell carcinoma (OSCC) [95, 96], hepatocellular carcinoma (HCC) [97,98,99,100], renal cell carcinoma (RCC) [101], bladder cancer [102], cervical squamous cell carcinoma(CSCC) [103], breast cancer [104,105,106], osteosarcoma [107], and non-small cell lung cancer (NSCLC) [108]. Furthermore, SLC16A1-AS1 exhibits multiple biological roles in these primary malignancies, highlighting its complexity in tumorigenesis and its potential as a tumor biomarker [93,94,95,96,97,98,99,100,101,102,103,104,105,106,107,108]. SLC16A1-AS1 is intricately linked to the proliferation, migration and invasion of tumor cells, and its abnormal expression is also related to the clinical characteristics and prognosis of cancer patients [93,94,95,96,97,98,99,100,101,102,103,104,105,106,107,108].

This article comprehensively reviews the latest findings on the role of SLC16A1-AS1 in a spectrum of human cancers, delving into its expression patterns and molecular mechanisms across different cancer types, and evaluating its viability as a prognostic and diagnostic marker. This review aims to enrich our understanding of the multifaceted role of SLC16A1-AS1 in oncology, highlighting its promise as a key biomarker and therapeutic target.

SLC16A1-AS1, a tumor-associated lncRNA recently uncovered, has exhibited dysregulated expression patterns across a range of cancer types, garnering considerable interest for its potential involvement in tumor development. In vitro and in vivo investigations have illuminated the multifaceted roles of SLC16A1-AS1 in oncogenesis. These studies, utilizing an array of cell-based assays, have probed its impact on crucial cellular activities, including proliferation, apoptosis, cell cycle regulation, migration, and invasion. Table 1 summarizes the expression patterns of SLC16A1-AS1 in various tumors, highlighting their relevant functional effects and roles in cancer progression. The subsequent sections explore in detail the specific functions and regulatory mechanisms of SLC16A1-AS1 in different tumors.

In glioblastoma, a notably aggressive form of brain tumor [109,110,111], SLC16A1-AS1 has been identified as playing a pivotal oncogenic role, as elucidated by in vitro studies. Research by Jin et al. [93] revealed that in glioblastoma cells, the lncRNA SLC16A1-AS1 regulates both mature and premature forms of miR-1269. This regulation is linked to significant changes in cancer cell behaviors, including proliferation, apoptosis, migration, and invasion, indicating SLC16A1-AS1’s role as an oncogene. Furthermore, Long et al. [94] complemented these findings by demonstrating that SLC16A1-AS1 is upregulated in glioblastoma and influences cancer cell proliferation through the epigenetic modification, specifically the methylation of miR-149. This interaction between SLC16A1-AS1 and miR-149 methylation further cements the role of SLC16A1-AS1 as an oncogene in glioblastoma. The distinct expression patterns and functional impacts of SLC16A1-AS1, involving crucial processes like microRNA regulation and methylation, not only advance our understanding of glioblastoma’s molecular mechanisms but also highlight the potential of SLC16A1-AS1 as a biomarker for glioblastoma, providing promising avenues for targeted cancer therapies and diagnostic strategies.

SLC16A1-AS1 plays a nuanced role in the pathogenesis of OSCC. Li et al. [95] delves into the interaction between SLC16A1-AS1 and miR-5088-5p (both mature and premature forms) in OSCC. This study indicates that SLC16A1-AS1 acts as a tumor suppressor by modulating the behavior of miR-5088-5p, which in turn affects cancer cell proliferation [95]. The specific mechanism through which SLC16A1-AS1 exerts this suppressive effect, particularly in relation to miR-5088-5p, highlights a complex interplay that could significantly influence OSCC progression.

In contrast, the findings of Feng et al. [96] portray SLC16A1-AS1 in a different light. This study does not specify an interaction with a particular miRNA but focuses on the broader tumorigenesis features of SLC16A1-AS1 in OSCC. Here, SLC16A1-AS1 is seen to contribute to cancer cell proliferation and cell cycle arrest, suggesting its role as an oncogene [96]. This oncogenic aspect of SLC16A1-AS1 in OSCC points to its potential involvement in accelerating cancer progression by disrupting normal cell cycle regulation.

These contrasting studies collectively indicate that SLC16A1-AS1 has a complex and dualistic role in OSCC. On one hand, it interacts with specific miRNAs like miR-5088-5p, potentially acting as a tumor suppressor. On the other hand, it exhibits characteristics of an oncogene, influencing cell proliferation and cell cycle processes. This duality underscores the intricate nature of SLC16A1-AS1’s involvement in OSCC and suggests that its role may vary depending on the molecular context and cellular environment. Understanding these dynamics is crucial for developing targeted therapeutic strategies for OSCC.

SLC16A1-AS1 exhibits a complex and significant role in HCC [97,98,99]. Tian et al. [97] reported that SLC16A1-AS1 is upregulated in HCC and is associated with poor patient survival, positioning it as a potential prognostic biomarker. Furthermore, SLC16A1-AS1’s interaction with miR-141 through methylation has been shown to promote cell proliferation, characterizing it as an oncogene. This oncogenic nature is further supported by the study of Duan et al. [99], which demonstrates that SLC16A1