2.1 Nonsolid tumors

Nonsolid tumors are a class of tumors that include leukemia, lymphoma, and myeloma. According to the latest global cancer survey data, leukemia accounts for 2.4% of global malignant tumors incidence and 3.1% of global malignant tumors mortality, posing a major threat to human health [1].

2.1.1 Acute myeloid leukemia (AML)

AMLis defined by the rapid proliferation of malignant myeloid stem cells within the bone marrow and is associated with increased clinical mortality rates [16]. Integrated analysis of TCGA and TARGET datasets revealed a marked reduction in SNHG29 expression among tumor cells from patients with AML with high-risk profiles relative to those with lower risk scores [17]. Consistent observations were reported in patients with FLT3-ITD AML whose prognosis was unfavorable, as SNHG29 expression was significantly downregulated [18]. Kaplan–Meier survival analysis further indicated that SNHG29 expression served as a prognostic indicator for OS in patients with AML [17]. As a tumor suppressor, SNHG29 modulates EP300 genomic binding via epigenetic mechanisms, alters EP300-driven histone modifications, and consequently regulates the expression of multiple downstream AML-associated genes, collectively suppressing the proliferation of FLT3-ITD AML cells [18]. These findings position SNHG29 as a potential biomarker for AML pathogenesis and progression and for diagnostic and prognostic assessment.

2.1.2 CML

CMLis characterized by an indolent onset that gradually advances to a blast phase if inadequately managed, resulting in poor clinical outcomes. Despite systemic therapy, a subset of patients exhibit therapeutic resistance, leading to treatment failure [19]. SNHG29 expression is markedly elevated in the peripheral blood of individuals with CML compared with healthy controls, and its upregulation is closely associated with disease progression. Elevated SNHG29 levels are correlated with advanced tumor stages and predict unfavorable prognosis in patients with CML [20]. These results position SNHG29 as a potential biomarker for both diagnostic and prognostic applications in clinical settings. Furthermore, functional assays demonstrated that SNHG29 knockdown suppressed CML cell proliferation while inducing apoptosis [14], suggesting a novel therapeutic strategy for disease management. Future research could focus on targeted therapy for SNHG29, inhibiting the expression of SNHG29 in CML tumor cells to suppress tumor cell proliferation and achieve therapeutic effects for CML patients.

2.1.3 ALL

ALLis characterized by the uncontrolled proliferation of immature lymphoid cells. The majority of cases arise in individuals without known risk factors, and only a limited subset exhibits identifiable triggers such as genetic predisposition or environmental influences [20], rendering early diagnosis particularly challenging. Analysis of the TARGET dataset revealed that SNHG29 was differentially expressed in the peripheral blood of patients with ALL compared with healthy controls. This functional enrichment indicates the involvement of SNHG29 in key oncogenic pathways, including the PI3K–Akt and p53 signaling pathways [21]. These expression patterns imply a potential role for SNHG29 in ALL pathogenesis and disease progression, highlighting its value as a candidate prognostic biomarker or therapeutic target that warrants further investigation.

2.2 Solid tumors2.2.1 Breast cancer

Breast cancer ranks as the second most frequently diagnosed malignancy after lung cancer and remains a leading cause of cancer-related death among women. The latest survey shows that the incidence and mortality of breast cancer account for 11.6% and 6.9% of global malignant tumors cases, respectively [1]. High mortality primarily stems from delayed detection and ineffective therapeutic interventions [22]. Early diagnostic measures and reliable approaches to assess treatment efficacy are essential for improving clinical outcomes. Elevated SNHG29 expression is correlated with chemoresistance and an unfavorable prognosis in patients with breast cancer. SNHG29 enhances resistance of breast cancer cells to chemotherapeutic agents through a series of signaling pathways and affects the prognosis of breast cancer patients [15]. Additionally, SNHG29 and its associated ceRNA network exert significant regulatory influences on tumor initiation and progression. SNHG29 expression levels have also been linked to patient prognosis in clinical settings [23]. Collectively, these data position SNHG29 as a molecular biomarker with diagnostic and prognostic relevance in breast cancer, while its involvement in chemoresistance highlights its potential as a therapeutic target. Future research could explore the use of targeted therapy against SNHG29 to reverse chemotherapy resistance in breast cancer tumor cells, thereby enhancing treatment outcomes for breast cancer patients.

2.2.2 Cervical cancer

Cervical cancer, a leading cause of malignancy-related death in women, has a high incidence rate. The latest research data shows that the incidence and mortality rates of cervical cancer are 3.3% and 3.6% of all malignant tumors worldwide, respectively [1]. Identifying reliable biomarkers for early diagnosis and prognosis prediction remains a critical area of research in this field [24]. A recent study revealed strong correlations between elevated SNHG29 expression and proliferation, migration, invasion, and EMT in cervical cancer cells. SNHG29 overexpression promotes these malignant behaviors of tumor cells, thereby facilitating cervical cancer progression [25]. A similar investigation revealed that SNHG29 overexpression in cervical cancer cells enhanced EMT. Additionally, animal studies have demonstrated that SNHG29 knockout inhibits both EMT and tumor cell proliferation [26]. These observations highlight the role of SNHG29 in cervical cancer pathogenesis, positioning it as a promising diagnostic biomarker and a potential therapeutic target for this malignancy. Further research could target SNHG29, which is highly expressed in cervical cancer cells, to block its tumor-promoting effects. Additionally, a risk model could be established based on the expression levels of SNHG29 in cervical cancer cells to predict treatment outcomes for cervical cancer patients.

2.2.3 Ovarian cancer

Ovarian cancer, a highly lethal malignancy, is frequently diagnosed at advanced stages, with many patients experiencing recurrence following initial surgery and chemotherapy. The need for novel diagnostic and therapeutic approaches remains critical [27]. Recent survey data show that the incidence and mortality of ovarian cancer account for 1.6% and 2.1% of global malignant tumors cases, respectively [1]. Elevated expression of SNHG29 in ovarian cancer cells has been linked to immunosuppression and poor patient prognosis. Specifically, SNHG29 suppresses the immune response through cell signaling pathways, contributing to adverse clinical outcomes in patients with ovarian cancer [28]. These results highlight SNHG29 as a promising prognostic biomarker and therapeutic target, suggesting its potential for future research in ovarian cancer treatment. In the future, targeted therapy against SNHG29 may be used to reverse its high expression and its immunosuppressive effect on ovarian cancer patients, thereby enhancing their antitumor immune capacity and improving their prognosis.

2.2.4 Glioblastoma

Recent global survey data show that the incidence and mortality of brain malignancies account for 1.6% and 2.6% of all malignant tumors worldwide, respectively [1]. Primary brain malignancies, particularly glioblastoma, have high mortality rates, with glioblastoma being the most aggressive form of primary brain malignancy. Current treatment approaches face near-inevitable tumor recurrence, with most patients succumbing to disease progression. Thus, accurate evaluation of treatment response and early prediction, along with timely detection of tumor progression or recurrence, are critical for improving patient outcomes [29, 30]. Evidence indicates that SNHG29 is overexpressed in glioblastoma, and it enhances tumor cell proliferation, migration, and EMT through cell signaling pathways, driving glioblastoma progression [31]. These findings highlight the potential of SNHG29 as a biomarker for early glioblastoma diagnosis and suggest that its involvement in tumor progression through cell signaling pathways may offer a promising therapeutic target for glioblastoma treatment. Further research can be conducted to investigate the relationship between SNHG29 expression levels and the progression of glioblastoma, thereby establishing a risk model to predict treatment outcomes for glioblastoma patients at an early stage. Additionally, further studies can explore the connection between SNHG29 and glioblastoma cell signaling pathways, enabling the application of SNHG29 in clinical targeted therapy.

2.2.5 Colorectal cancer

Colorectal cancer, a gastrointestinal malignancy with high morbidity and mortality, ranks among the leading causes of cancer-related death globally. The latest global data shows that the incidence and mortality rates of colorectal cancer are 9.6% and 9.3% of all malignant tumors worldwide, respectively [1]. The prognosis for patients in advanced stages is particularly poor, but the incidence of early-onset colorectal cancer has increased in recent years [32, 33]. These trends emphasize the urgent need to explore novel diagnostic and therapeutic strategies for early-stage detection and treatment. Research has demonstrated that SNHG29 is markedly underexpressed in colorectal cancer tissues. Moreover, its knockout significantly enhances the proliferation, metastasis, invasion, and colony formation of colorectal cancer cells [34]. This evidence suggests that SNHG29 may function as a tumor suppressor gene, with potential applications as a biomarker for both the diagnosis and treatment of colorectal cancer. Additionally, inhibiting SNHG29 expression has been shown to downregulate PD-L1 expression, thereby promoting antitumor immune responses [35]. These observations implicate SNHG29 in immunotherapy and position it as a promising target for therapeutic intervention. Further research is needed to clarify the relationship between SNHG29 expression levels and the development of colorectal cancer. Future studies could focus on the connection between SNHG29 and immunotherapy, using targeted therapy against SNHG29 to enhance the efficacy of immunotherapy for colorectal cancer and thereby improve patient outcomes.

2.2.6 Laryngeal carcinoma

Laryngeal carcinoma, a prevalent malignancy of the head and neck, continues to pose a significant threat to human health, despite recent declines in its incidence and mortality rates. Recent surveys show that the incidence and mortality rates of laryngeal cancer are 0.9% and 1.1% of all malignant tumors worldwide, respectively [1]. It remains the most common type of head and neck cancer, highlighting the need for further advancements in early diagnosis and treatment [36, 37]. A recent study demonstrated that SNHG29 expression was downregulated in laryngeal carcinoma tissues and cells. This reduction in SNHG29 expression inhibited the proliferation, migration, and invasion of laryngeal carcinoma cells and suppressed the EMT process. Additionally, decreased SNHG29 expression is correlated with differentiation, T stage, lymph node metastasis, and advanced clinical stage, suggesting that SNHG29 significantly affects the initiation and progression of laryngeal carcinoma [38]. These data suggest that SNHG29 may serve as a novel biomarker for diagnosing, treating, and predicting the prognosis of patients with laryngeal carcinoma, warranting further investigation. In the future, further exploration of the correlation between SNHG29 expression levels and the occurrence and development of laryngeal cancer can be conducted. With more research data, predictive models can be established and further applied to the diagnosis and prognosis of clinical laryngeal cancer patients.

2.2.7 Other solid tumorsSNHG29 is overexpressed in gastrointestinal stromal tumors (GISTs) [12] and osteosarcoma [11]. Additionally, a study revealed a positive correlation between SNHG29 expression and GIST diameter, suggesting its potential role as an oncogene in these tumors [12]. These observations highlight the dysregulation of SNHG29 in various malignancies and its significant association with tumor progression. Given the implications of this dysregulation, further investigation is warranted to fully explore the research potential of SNHG29.