Exploring the multifaceted role of GCN1: Implications in cellular responses and disease pathogenesis.

GCN1 is a highly conserved protein present widely across eukaryotes. As an upstream activator of protein kinase GCN2, GCN1 plays a pivotal role in integrated stress responses, such as amino acid starvation and oxidative stress. Through interaction with GCN2, GCN1 facilitates the activation of GCN2, thus initiating downstream signaling cascades in response to cellular stressors. In these contexts, the activation of GCN2 necessitates the presence and action of GCN1. Notably, GCN1 also operates as a ribosome collision sensor, contributing significantly to the translation quality control pathway. These discoveries offer valuable insights into cellular responses to internal stresses, vital for maintaining cellular homeostasis. Additionally, GCN1 exhibits the ability to regulate the cell cycle and suppress inflammation, among other processes, independently of GCN2. Our review outlines the structural characteristics and biological functions of GCN1, shedding light on its significant involvement in the onset and progression of various cancer and non-cancer diseases. Our work underscores the role of GCN1 in the context of drug therapeutic effects, hinting at its potential as a promising drug target. Furthermore, our work delves deep into the functional mechanisms of GCN1, promising innovative avenues for the diagnosis and treatment of diseases in the future. The exploration of GCN1's multifaceted roles not only enhances our understanding of its mechanisms but also paves the way for novel therapeutic interventions. The ongoing quest to unveil additional functions of GCN1 holds the promise of further enriching our comprehension of its mode of action.

Unveiling the role of tRNA-derived small RNAs in MAPK signaling pathway: implications for cancer and beyond.

tRNA-derived small RNAs (tsRNAs) are novel small non-coding RNAs originating from mature or precursor tRNAs (pre-tRNA), typically spanning 14 to 30 nt. The Mitogen-activated protein kinases (MAPK) pathway orchestrates cellular responses, influencing proliferation, differentiation, apoptosis, and transformation. tsRNAs influence the expression of the MAPK signaling pathway by targeting specific proteins within the pathway. Presently, four MAPK-linked tsRNAs have implications in gastric cancer (GC) and high-grade serous ovarian cancer (HGSOC). Notably, tRF-Glu-TTC-027 and tRF-Val-CAC-016 modulate MAPK-related protein expression, encompassing p38, Myc, ERK, CyclinD1, CyclinB, and c-Myc, hindering GC progression via MAPK pathway inhibition. Moreover, tRF-24-V29K9UV3IU and tRF-03357 remain unexplored in specific mechanisms. KEGG analysis posits varied tsRNAs in MAPK pathway modulation for diverse non-cancer maladies. Notably, high tRF-36-F900BY4D84KRIME and tRF-23-87R8WP9IY expression relates to varicose vein (VV) risk. Elevated tiRNA-Gly-GCC-001, tRF-Gly-GCC-012, tRF-Gly-GCC-013, and tRF-Gly-GCC-016 target spinal cord injury (SCI)-related brain-derived neurotrophic factor (BDNF), influencing MAPK expression. tRF-Gly-CCC-039 associates with diabetes foot sustained healing, while tRF-5014a inhibits autophagy-linked ATG5 in diabetic cardiomyopathy (DCM). Additionally, tsRNA-14783 influences keloid formation by regulating M2 macrophage polarization. Upregulation of tRF-Arg-ACG-007 and downregulation of tRF-Ser-GCT-008 are associated with diabetes. tsRNA-04002 alleviates Intervertebral disk degeneration (IDD) by targeting PRKCA. tsRNA-21109 alleviates Systemic lupus erythematosus (SLE) by inhibiting macrophage M1 polarization. The upregulated tiNA-Gly-GCC-002 and the downregulated tRF-Ala-AGC-010, tRF-Gln-CTG-005 and tRF-Leu-AAG-001 may be involved in the pathogenesis of Lupus nephritis (LN) by affecting the expression of MAPK pathway. Downregulation of tsRNA-1018, tsRNA-3045b, tsRNA-5021a and tsRNA-1020 affected the expression of MAPK pathway, thereby improving Acute lung injury (ALI). This review comprehensively dissects tsRNA roles in MAPK signaling across cancers and other diseases, illuminating a novel avenue for translational medical exploration.

CLLU1 as an emerging biomarker in chronic lymphoid leukemia.

CLLU1, a disease-specific gene associated with chronic lymphoid leukemia (CLL), is located on chromosome 12q22. Previous studies considered CLLU1 to be a non-coding RNA; however, recent research has discovered that its coding sequence region possesses the potential to encode a short peptide similar to interleukin-4. Remarkably, abnormally elevated expression of CLLU1 has only been detected in chronic lymphoid leukemia among all hematological cancers. High CLLU1 expression often indicates more malignant pathological features and an unfavorable prognosis for patients. Importantly, the expression level of CLLU1 remains unaffected by the passage of time or therapeutic interventions, thus rendering it a novel prognostic marker. This article provides a comprehensive summary of relevant research findings on CLLU1 in the context of CLL prognosis and clinical applications, aiming to guide subsequent theoretical and clinical investigations in this field.

Cuproptosis-associated ncRNAs predict breast cancer subtypes.

BACKGROUND: Cuproptosis is a novel copper-dependent mode of cell death that has recently been discovered. The relationship between Cuproptosis-related ncRNAs and breast cancer subtypes, however, remains to be studied. METHODS: The aim of this study was to construct a breast cancer subtype prediction model associated with Cuproptosis. This model could be used to determine the subtype of breast cancer patients. To achieve this aim, 21 Cuproptosis-related genes were obtained from published articles and correlation analysis was performed with ncRNAs differentially expressed in breast cancer. Random forest algorithms were subsequently utilized to select important ncRNAs and build breast cancer subtype prediction models. RESULTS: A total of 94 ncRNAs significantly associated with Cuproptosis were obtained and the top five essential features were chosen to build a predictive model. These five biomarkers were differentially expressed in the five breast cancer subtypes and were closely associated with immune infiltration, RNA modification, and angiogenesis. CONCLUSION: The random forest model constructed based on Cuproptosis-related ncRNAs was able to accurately predict breast cancer subtypes, providing a new direction for the study of clinical therapeutic targets.

LINC00319: Unraveling the spectrum from gene regulation to clinical applications in cancer progression.

LncRNAs are RNA transcripts that exceed 200 nucleotides in length and do not encode proteins. LINC00319 is a type of lncRNA that is highly expressed in various cancers and is regulated by CCL18 and MYC. High levels of LINC00319 are associated with poorer prognosis and more malignant clinical features in cancer patients. LINC00319 can regulate the expression of downstream genes, including 2 protein-coding genes and 11 miRNAs. It participates in controlling three signaling pathways and various cellular behaviors. LINC00319 and its downstream genes are potential targets for cancer therapy and are associated with common cancer treatments. This article reviews the abnormal expression of LINC00319 in human cancers and related molecular mechanisms, providing clues for further diagnosis and treatment.

Current insights into the oncogenic roles of lncRNA LINC00355.

Long noncoding RNAs (lncRNAs) are a class of nonprotein-coding transcripts that are longer than 200 nucleotides. LINC00355 is a lncRNA located on chromosome 13q21.31 and is consistently upregulated in various cancers. It regulates the expression of downstream genes at both transcriptional and posttranscriptional levels, including eight microRNAs (miR-15a-5p, miR-34b-5p, miR-424-5p, miR-1225, miR-217-5p, miR-6777-3p, miR-195, and miR-466) and three protein-coding genes (ITGA2, RAD18, and UBE3C). LINC00355 plays a role in regulating various biological processes such as cell cycle progression, proliferation, apoptosis, epithelial-mesenchymal transition, invasion, and metastasis of cancer cells. It is involved in the regulation of the Wnt/ß-catenin signaling pathway and p53 signaling pathway. Upregulation of LINC00355 has been identified as a high-risk factor in cancer patients and its increased expression is associated with poorer overall survival, recurrence-free survival, and disease-free survival. LINC00355 upregulation has been linked to several unfavorable clinical characteristics, including advanced tumor node metastasis and World Health Organization stages, reduced Karnofsky Performance Scale scores, increased tumor size, greater depth of invasion, and more extensive lymph node metastasis. LINC00355 induces chemotherapy resistance in cancer cells by regulating five downstream genes, namely HMGA2, ABCB1, ITGA2, WNT10B, and CCNE1 genes. In summary, LINC00355 is a potential oncogene with great potential as a diagnostic marker and therapeutic target for cancer.

Disulfidptosis-associated lncRNAs predict breast cancer subtypes.

Disulfidptosis is a newly discovered mode of cell death. However, its relationship with breast cancer subtypes remains unclear. In this study, we aimed to construct a disulfidptosis-associated breast cancer subtype prediction model. We obtained 19 disulfidptosis-related genes from published articles and performed correlation analysis with lncRNAs differentially expressed in breast cancer. We then used the random forest algorithm to select important lncRNAs and establish a breast cancer subtype prediction model. We identified 132 lncRNAs significantly associated with disulfidptosis (FDR < 0.01, |R|> 0.15) and selected the first four important lncRNAs to build a prediction model (training set AUC = 0.992). The model accurately predicted breast cancer subtypes (test set AUC = 0.842). Among the key lncRNAs, LINC02188 had the highest expression in the Basal subtype, while LINC01488 and GATA3-AS1 had the lowest expression in Basal. In the Her2 subtype, LINC00511 had the highest expression level compared to other key lncRNAs. GATA3-AS1 had the highest expression in LumA and LumB subtypes, while LINC00511 had the lowest expression in these subtypes. In the Normal subtype, GATA3-AS1 had the highest expression level compared to other key lncRNAs. Our study also found that key lncRNAs were closely related to RNA methylation modification and angiogenesis (FDR < 0.05, |R|> 0.1), as well as immune infiltrating cells (P.adj < 0.01, |R|> 0.1). Our random forest model based on disulfidptosis-related lncRNAs can accurately predict breast cancer subtypes and provide a new direction for research on clinical therapeutic targets for breast cancer.

Current status and future perspectives in dysregulated miR-492.

MicroRNAs (miRNAs) are a class of single-stranded small non-coding RNAs with a length of 21-23 nucleotides. One such miRNA, miR-492, is located in the KRT19 pseudogene 2 (KRT19P2) of chromosome 12q22 and can also be generated from the processing of the KRT19 transcript at chromosome 17q21. Aberrant expression of miR-492 has been observed in cancers of various physiological systems. miR-492 has been shown to target at least 11 protein-coding genes, which are involved in the regulation of cellular behaviors such as growth, cell cycle, proliferation, epithelial- mesenchymal transition (EMT), invasion and migration. The expression of miR-492 can be regulated by both endogenous and exogenous factors. Furthermore, miR-492 is involved in the regulation of several signaling pathways including the PI3K/AKT signaling pathway, WNT/ß-catenin signaling pathway, and MAPK signaling pathway. High expression of miR-492 has been closely associated with shorter overall survival in patients with gastric cancer, ovarian cancer, oropharyngeal carcinoma, colorectal cancer, and hepatocellular carcinoma. This study systematically summarizes the related research findings on miR-492, providing potential insights for future investigations.

The tumor suppressor role and ceRNA network of miR-1294 in cancer.

miRNAs are endogenous small RNAs that are important regulators of gene expression. miR-1294 was found to be significantly down-regulated in 15 cancers and regulated by 21 upstream regulators. miR-1294 affects the proliferation, migration, invasion, and apoptosis of cancer cells. The target genes of miR-1294 are involved in the PI3K/AKT/mTOR, RAS, and JAK/STAT signaling pathways. Six target genes of miR-1294 are the targets of a variety of drugs. Low expression of miR-1294 is associated with resistance to cisplatin and TMZ and a poorer prognosis in patients with ESCC, GC, EOC, PDAC, or NSCLC. Therefore, this work outlines the molecular mechanisms and provides a basis for the clinical significance of the tumor suppressor miR-1294 in cancer.

Targeting the p53 signaling pathway in cancers: Molecular mechanisms and clinical studies.

Tumor suppressor p53 can transcriptionally activate downstream genes in response to stress, and then regulate the cell cycle, DNA repair, metabolism, angiogenesis, apoptosis, and other biological responses. p53 has seven functional domains and 12 splice isoforms, and different domains and subtypes play different roles. The activation and inactivation of p53 are finely regulated and are associated with phosphorylation/acetylation modification and ubiquitination modification, respectively. Abnormal activation of p53 is closely related to the occurrence and development of cancer. While targeted therapy of the p53 signaling pathway is still in its early stages and only a few drugs or treatments have entered clinical trials, the development of new drugs and ongoing clinical trials are expected to lead to the widespread use of p53 signaling-targeted therapy in cancer treatment in the future. TRIAP1 is a novel p53 downstream inhibitor of apoptosis. TRIAP1 is the homolog of yeast mitochondrial intermembrane protein MDM35, which can play a tumor-promoting role by blocking the mitochondria-dependent apoptosis pathway. This work provides a systematic overview of recent basic research and clinical progress in the p53 signaling pathway and proposes that TRIAP1 is an important therapeutic target downstream of p53 signaling.

Aberrant expression of microRNA-4443 (miR-4443) in human diseases.

miRNA is a small endogenous RNA and an important regulator of gene expression. miR-4443 is abnormally expressed in 12 diseases including cancer. The expression of miR-4443 is regulated by 3 upstream factors. miR-4443 has 12 downstream target genes. miR-4443 inhibits the expression of its target genes, thereby affecting the migration, proliferation, and invasion of pathological cells. miR-4443 participates in 4 signaling pathways and plays a role in the occurrence and development of several diseases. In addition, miR-4443 can also promote resistance to multiple drugs. Here, this article summarizes the aberrant expression of miR-4443 and its pathogenic molecular mechanisms in human diseases, which provides clues and directions for the follow-up research of miR-4443.

Dysregulation of miR-4443 affects the behaviors of diseased cells.miR-4443 is involved in the regulation of four signaling pathways.miR-4443 is associated with reduced drug sensitivity in cancer patients.

Novel Insights into miR-944 in Cancer.

miRNA is a class of endogenous short-chain non-coding RNAs consisting of about 22 nucleotides. miR-944 is located in the fourth intron of the TP63 gene in the 3q28 region. miR-944 is abnormally expressed in cancers in multiple systems including neural, endocrine, respiratory, reproductive, and digestive systems. miR-944 can target at least 27 protein-coding genes. miR-944 can regulate a series of cell behaviors, such as cell cycle, proliferation, invasion and migration, EMT, apoptosis, etc. miR-944 participates in the networks of 11 ceRNAs, including six circRNAs and five lncRNAs. miR-944 is involved in three signaling pathways. The abnormal expression of miR-944 is closely related to the clinicopathological conditions of various cancer patients. Deregulated expression of miR-944 is significantly associated with clinicopathology and prognosis in cancer patients. In addition, miR-944 is also associated with the development of DDP, RAPA, DOX, and PTX resistance in cancer cells. miR-944 is involved in the anticancer molecular mechanisms of matrine and Rhenium-liposome drugs. In conclusion, this work systematically summarizes the related findings of miR-944, which will provide potential hints for follow-up research on miR-944.

Dysfunction and ceRNA network of the tumor suppressor miR-637 in cancer development and prognosis.

MicroRNAs (miRNAs) are a class of small non-coding RNAs ranging from 17 to 25 nt in length. miR-637 is down-regulated in most cancers and up-regulated only in clear cell renal cell carcinoma (ccRCC). miR-637 can target 21 protein-coding genes, which are involved in the regulation of cell growth, cell cycle, cell proliferation, epithelial-mesenchymal transition (EMT), cancer cell invasion and metastasis, etc. In glioma, the transcription factor ZEB2 can bind to the miR-637 promoter region and inhibit miR-637 expression. Besides, miR-637 could be negatively regulated by competing endogenous RNA (ceRNAs) comprising 13 circular RNA (circRNAs) and 9 long non-coding RNA (lncRNAs). miR-637 is involved in regulating five signaling pathways, including the Jak/STAT3, Wnt/ß-catenin, PI3K/AKT, and ERK signaling pathways. Low miR-637 expression was significantly associated with larger tumors and later tumor node metastasis (TNM) staging in cancer patients. Low miR-637 expression was also associated with poorer overall survival (OS) in cancer patients such as glioblastoma and low-grade gliomas (GBM/LGG), non-small cell lung cancer (NSCLC), hepatocellular carcinoma (HCC), and ovarian cancer (OV). Low expression of miR-637 increases the resistance of colorectal cancer (CRC) and human cholangiocarcinoma (CHOL) cancer cells to three anticancer chemotherapeutics (gemcitabine (dFdC), cisplatin (DDP), and oxaliplatin (OXA)). Our work summarizes the abnormal expression of miR-637 in various cancers, expounds on the ceRNA regulatory network and signaling pathway involved in miR-637, and summarizes the effect of its abnormal expression on the biological behavior of tumor cells. At the same time, the relationship between the expression levels of miR-637 and its related molecules and the prognosis and pathological characteristics of patients was further summarized. Finally, our work points out the insufficiency of miR-637 in current studies and is expected to provide potential clues for future miR-637-related studies.

Emerging role of LINC00461 in cancer.

LINC00461 is located in the intergenic region between the protein-coding genes MEF2C and TMEM161B. LINC00461 upregulation was associated with the risk of 13 tumors and was strongly associated with clinicopathologic features and poor prognosis in 11 tumors. LINC00461 is involved in resistance to four anticancer drugs, including sunitinib for renal cell carcinoma, cisplatin for head and neck squamous cell carcinoma and rectal cancer, temozolomide for glioma, and docetaxel for breast cancer. LINC00461 can sponge 18 miRNAs to form a complex ceRNA network that regulates the expression of a large number of downstream genes. LINC00461 is involved in the MAPK/ERK signaling pathway and PI3K/AKT signaling pathway, thereby promoting tumorigenesis. Notably, knockdown of LINC00461 in exosomes antagonizes tumor cell proliferation in multiple myeloma. This article summarizes the diagnostic, prognostic, and therapeutic value of LINC00461 in various tumors, and systematically describes the ceRNA network and signaling pathways associated with LINC00461, providing potential directions for future LINC00461 research.

LINC00665: An Emerging Biomarker for Cancer Diagnostics and Therapeutics.

Long intergenic noncoding RNA 00665 (LINC00665) is located on human chromosome 19q13.12. LINC00665 was upregulated in eighteen cancers and downregulated in two cancers. LINC00665 not only inhibits 25 miRNAs but also directly affects the stability of ten protein-coding genes. Notably, LINC00665 also encodes a micro-peptide CIP2A-BP that promotes triple-negative breast cancer progression. LINC00665 can participate in five signaling pathways to regulate cancer progression, including the Wnt/ß-catenin signaling pathway, TGF-ß signaling pathway, NF-κB signaling pathway, PI3K/AKT signaling pathway, and MAPK signaling pathway. Aberrant expression of LINC00665 in breast cancer, gastric cancer, and hepatocellular carcinoma can be used for disease diagnosis. In addition, aberrant expression of LINC00665 is closely associated with clinicopathological features and poor prognosis of various cancers. LINC00665 is closely associated with the effects of anticancer drugs, including gefitinib and cisplatin in non-small cell lung cancer, gemcitabine in cholangiocarcinoma, and cisplatin-paclitaxel in breast cancer. This work systematically summarizes the diagnostic and prognostic values of LINC00665 in various tumors, and comprehensively analyzes the molecular regulatory mechanism related to LINC00665, which is expected to provide clear guidance for future research.

LINC00963: A potential cancer diagnostic and therapeutic target.

Long intergenic noncoding RNA 00963 (LINC00963) is located on human chromosome 9q34.11. Aberrantly expressed LINC00963 often exerts oncogenic effects by regulating various cellular processes including proliferation, migration, invasion, EMT, and apoptosis. Overexpressed LINC00963 is associated with cancer clinicopathological features and poor cancer prognosis, and can be used in the diagnosis of hepatocellular carcinoma. LINC00963 can build a complex ceRNA network by competitively binding to 22 miRNAs in 14 cancers. LINC00963 can also directly regulate four downstream protein-coding genes. Specifically, LINC00963 promotes the transition of prostate cancer from an androgen-dependent mode to an androgen-independent mode by participating in the transactivation of EGFR. LINC00963 can bind EZH2 and inhibit p21 expression, thereby promoting glioma cell proliferation and invasion. In non-small cell lung cancer, LINC00963 can recruit NONO and CRTC, forming a positive feedback loop of LINC00963/NONO/CRTC/CREB/LINC00963, thereby promoting cancer cell metastasis. LINC00963 is involved in the PI3K/AKT signaling pathway, Wnt signaling pathway, AMPK signaling pathway, and MAPK signaling pathway. Furthermore, LINC00963 is associated with drug resistance in oral squamous cell carcinoma (cisplatin and 5-fluorouracil) and gastric cancer (oxaliplatin) and predicts neoadjuvant efficacy of taxane-anthracyclines in breast cancer. This work systematically reviewed the clinical value of abnormal expression of LINC00963 in various tumors, demonstrated the complex molecular mechanism of LINC00963, and provided directions for future related research.

miR-1908 Dysregulation in Human Cancers.

MiR-1908 is a miRNA located in the intron of the fatty acid desaturase 1 (FADS1) gene. The expression level of miR-1908 is abnormal in many diseases such as cancer. miR-1908 can inhibit the expression of at least 27 target genes by binding to the 3' untranslated region (3' UTR) of target genes. miR-1908 is involved in the biological processes of cell proliferation, cell differentiation, cell apoptosis, cancer cell invasion, and metastasis. The expression of miR-1908 is regulated by 11 factors, including lncRNA HOTTIP, adipokines (TNF-α, leptin, and resistin), NF-κB, free fatty acid (FFA), cholesterol, stearoyl-CoA desaturase (SCD1), immune-related transcription factors (STAT1, RB1, and IRF1). The expression of miR-1908 is also affected by the anticancer drug OSW-1, growth hormone (GH), and the anticonvulsant drug sodium valproate. In addition, the aberrant expression of miR-1908 is also related to the prognosis of a variety of cancers, including non-small cell lung cancer (NSCLC), ovarian cancer (OC), breast cancer, cervical cancer, glioma, high-grade serous ovarian carcinoma (HGSOC), osteosarcoma, etc. This article summarizes the abnormal expression pattern of miR-1908 in various diseases and its molecular regulation mechanisms. Our work will provide potential hints and direction for future miR-1908-related research.

LINC00520: A Potential Diagnostic and Prognostic Biomarker in Cancer.

Long non-coding RNA (lncRNA) is important in the study of cancer mechanisms. LINC00520 is located on human chromosome 14q22.3 and is a highly conserved long non-coding RNA. LINC00520 is widely expressed in various tissues. The expression of LINC00520 is regulated by transcription factors such as Sp1, TFAP4, and STAT3. The high expression of LINC00520 is significantly related to the risk of 11 cancers. LINC00520 can competitively bind 10 miRNAs to promote tumor cell proliferation, invasion, and migration. In addition, LINC00520 is involved in the regulation of P13K/AKT and JAK/STAT signaling pathways. The expression of LINC00520 is significantly related to the clinicopathological characteristics and prognosis of tumor patients and is also related to the sensitivity of HNSCC to radiotherapy. Here, this article summarizes the abnormal expression pattern of LINC00520 in cancer and its potential molecular regulation mechanism and points out that LINC00520 can be used as a potential biomarker for cancer diagnosis, prognosis, and treatment.

Dysregulation of miR-411 in cancer: Causative factor for pathogenesis, diagnosis and prognosis.

MiRNA accounts for 1-3% of genes but regulates more than 30% of gene expression in humans. This article analyzes the current deficiencies and challenges of miR-411 research and looks forward to the prospects of miR-411 in cancer. MiR-411 is a non-coding RNA located on chromosome 14. MiR-411 is abnormally expressed in a variety of cancers. The dysregulation of miR-411 can affect cancer cell proliferation, invasion, migration, apoptosis, colony formation, etc. miR-411 can be regulated by different lncRNAs and circRNAs. By targeting multiple genes, miR-411 participates in the activation of the MAPK signaling pathway, PI3K/AKT/mTOR signaling pathway, p53 signaling pathway, Ras signaling pathway, NF-κB signaling pathway, and Wnt/ß-catenin signaling pathway. The expression of miR-411 is related to the diagnosis, prognosis, and sensitivity of drugs in cancer patients. In conclusion, this work outlines the molecular mechanisms and cellular functions of aberrant expression of miR-411 and its target genes in cancer to reveal its potential value in diagnosis, prognosis, and drug sensitivity.

LINC00324 in cancer: Regulatory and therapeutic implications.

LINC00324 is a 2082 bp intergenic noncoding RNA. Aberrant expression of LINC00324 was associated with the risk of 11 tumors and was closely associated with clinicopathological features and prognostic levels of 7 tumors. LINC00324 can sponge multiple miRNAs to form complex ceRNA networks, and can also recruit transcription factors and bind RNA-binding protein HuR, thereby regulating the expression of a number of downstream protein-coding genes. LINC00324 is involved in 4 signaling pathways, including the PI3K/AKT signaling pathway, cell cycle regulatory pathway, Notch signaling pathway, and Jak/STAT3 signaling pathway. High expression of LINC00324 was associated with larger tumors, a higher degree of metastasis, a higher TNM stage and clinical stage, and shorter OS. Currently, four downstream genes in the LINC00324 network have targeted drugs. In this review, we summarize the molecular mechanisms and clinical value of LINC00324 in tumors and discuss future directions and challenges for LINC00324 research.