Lung cancer is predominant worldwide and its incidence rate is the highest in men and the second in women (Bade and Dela Cruz, 2020; Chen et al., 2021; Ma et al., 2021; Yuan et al., 2021). Zeng et al. (2020) showed that LINC01116 was overexpressed in LC tumor tissues compared to normal adjacent tissues. LINC01116 expression is high in LC patients, and they generally have more unsatisfactory outcomes than the others. Thus, previous reports have suggested that LINC01116 is an independent prognostic factor in LC. Furthermore, the expression of LINC01116 was shown to be high in patients with advanced tumor stages. For instance, recent studies showed that a considerable number of patients with low expression of LINC01116 were generally diagnosed with TNM I rather than TNM I/III. These results indicate that LINC01116 can be considered as a latent regulator that participates in the progression of metastasis and invasiveness in LC (Shang et al., 2021). Additionally, silencing of LINC01116 reverses this effect. Eventually, LINC01116 plays crucial roles in tumor processes and could provide an orientation for being diagnostic and prognostic markers of LC, but its actual situation of clinical application still requires massive clinical and basic research.

Gastric cancer is the 4th most prevalent malignant tumor. Due to the lack of early diagnostic markers, patients are commonly diagnosed at terminal stages, with tumors that have metastasized to proximal or even remote regions in the body (Lin et al., 2019; Arnold et al., 2020; Ascherman et al., 2021; Puliga et al., 2021). Su et al. (2019) discovered that LINC01116 and CASC11 were upregulated in GC tissues, compared with cancer-adjacent tissues, and were positively correlated with clinical stages. In addition, the overexpression of LINC01116 and CASC11 was found to collectively increase the migration and invasion of GC cells. In contrast, low expression of LINC01116 was found to be associated with suppressed metastasis and invasiveness in GC patients. Moreover, CASC11 silencing alleviated the overexpression of LINC01116. Additionally, Chen et al. (2020c) demonstrated that patients with abundant expression of LINC01116 in GC cells generally have shorter survival time than those with low expression levels, and that the inhibition of LINC01116 expression could impede the proliferation of GC cells. These findings provide a novel direction for the diagnosis and treatment of GC.

Colorectal cancer is the frequent cancer globally and has high mortality and incidence rates (Wieszczy et al., 2020; Świerczyński et al., 2021; Zaborowski et al., 2021; Zhao et al., 2021). Bi et al. (2020) revealed that LINC01116 was highly expressed in CRC tissues compared to normal tissues, and patients with high expression of LINC01116 had a very poor prognosis. LINC01116 knockdown substantially prevented the migration, proliferation, and invasion of CRC cells and activated cell apoptosis. Emerging evidence showed that a large number of patients were commonly diagnosed at terminal stages with high expression of LINC01116. Liang et al. (2021) identified that LINC01116 facilitated the growth of CRC cells and tumorigenicity through the downregulation of TPM1 expression. Specifically, LINC01116 can bind with EZH2 to accelerate the methylation of TPM1, which blocks the transcription of TPM1. Additionally, low expression of LINC01116 considerably impeded the tumorigenicity and angiogenesis of CRC cells in nude mice. Despite LINC01116 could serve as a diagnostic biomarker for in CRC, the deficiency of clinical application needs to be further investigated. For instance, researches of LINC01116 participated in CRC are only tested in tissues, and diverse effects between LINC01116 and molecular target markers are supposed to be probed in blood and other body fluids.

Brain gliomas are the most common primary malignant tumors in the central nervous system, presenting with an increasing mortality rate. Several patients present with an OS time of less than 2 years (Mondal and Kulshreshtha, 2021; Petridis et al., 2021; Tanabe et al., 2021; Tu et al., 2021). Wang et al. (2020c) found that the upregulation of LINC01116 in glioma cells is related to poor prognosis. When LINC01116 is knocked, G1-G0 phase arrest in Ln229 and U87 cells might be induced. Therefore, the apoptosis of glioma could be significantly inhibited. Moreover, LINC01116 has been shown to stimulate IL-1β transcription to generate an army of cytokines, which are associated with tumorigenicity via DDX5. Wang et al. (2020c) showed that LINC01116 positively regulates MDM2 to repress the p53 pathway, which activates the development of glioma cells. Current research shows that LINC01116 can substantially promote the proliferation and invasion abilities of glioma cells (Cole et al., 1986). Ye et al. revealed that LINC01116 expression is higher in glioma tissues than in normal tissues, and it could elevate the capacity of the cell cycle and cell proliferation by regulating the expression of VEGFA. In summary, these findings further clarify the biological functions of LINC01116 in glioma tumorigenesis and provide a promising treatment target for glioma patients.

Osteosarcoma is a leading cause of cancer-related death among young adolescents. Osteosarcoma patients retain high levels of metastasis and recurrence, accounting for approximately 30%–40% of cases (Lu et al., 2020; Zheng et al., 2020; Li et al., 2021c; Liu et al., 2021b). Zhang et al. (2019) reported that LINC01116 might remarkably accelerate the proliferation, migration, and invasion of osteosarcoma cells, but substantially precludes cell apoptosis. These results corroborated that LINC01116 directly interacted with EZH2 to mediate PTEN and p53. Thus, EZH2 knockdown reverses the LINC01116 functional effect on osteosarcoma cells (Zhang et al., 2019). Zhang et al. (2018) silenced LINC01116, inhibiting the viability of osteosarcoma cells and promoting cell apoptosis. Moreover, high expression of LINC01116 in patients generally results in a poorer prognosis. These results revealed a crucial role for LINC01116 in osteosarcoma. However, further investigation is required before clinical application.

Wu et al. (2020) shed new light on the silencing of LINC01116, which was shown to inhibit the tumorigenicity of OSCC through the upregulation of miRNA-136. Likewise, LINC01116 knockdown was shown to decrease the migration and invasion of HNSC cells, probably via the epithelial-mesenchymal transition pathway (Xing et al., 2020). Yu et al. (2021) suggested that LINC01116 was an oncogene that accelerates the development of prostate adenocarcinoma (PRAD) cells. Fang et al. (2018) reported that the proliferation and migration of EOC cells was increased with the overexpression of LINC01116. Knockdown of LINC01116 could function as an essential suppressor to block the viability and cloning ability of BC cells (Hu et al., 2018). Consequently, LINC01116 is a promising prognostic and therapeutic target for OSCC, HNSC, PRAD, EOC, and BC.

Proliferation of cancer cells generally occurs rapidly, which markedly affects the prognosis of patients (Liu et al., 2019; Zhang et al., 2020). A recent study validated that miR-744-5p might be a novel target of LINC01116 in lung (LAD). miR-744-5p was known as the suppressor to involving in malignant tumors and negatively through regulating CDCA4. Knockdown of miR-744-5p could promote tumor cell proliferation and migration in LAD. LINC01116 could mediate the expression of CDCA4 by competitively binding the sites of CDCA4 with miR-744-5p, which markedly increased cell growth in LAD (Ren et al., 2021)Numerous experiments have shown that LINC01116 is overexpressed in small cell lung carcinoma (SCLC) and that it could upregulate STAT3 to boost SCLC cell invasion and migration. However, high expression of miR-93-5p suppresses the effect of LINC01116 overexpression. Thus, LINC01116 is likely to modulate miR-93-5p, which contributes to the expression levels of STAT3 (Figure 3). However, high expression of miR-93-5p and LINC01116 did not exert an influence on mutual expression, implying that miR-93-5p might have other targets (Xiang et al., 2017). In osteosarcoma cells, LINC01116 was shown to accelerate cell proliferation by targeting miR-520a-3p and upregulating IL6R (Zhang et al., 2018). Similarly, Liu et al. showed that LINC01116 interacts with CASC11, which regulates the invasion and migration of GC cells (Figure 4). Accumulating evidence suggests that miR-145 might bridge the interaction between LINC01116 and CASC11 (Su et al., 2019).

In nasopharyngeal carcinoma (NPC) cells, LINC01116 was shown to induce the translation of MYC and enhance the expression of MYC protein, which plays an essential role in proliferation. Likewise, when MYC remains highly expressed, the effect of LINC01116 deletion can be recovered to some degree (Tran et al., 2016). In CRC cells, LINC01116 negatively correlates with miR-9-5p regulation, promoting the proliferation, invasion, and migration of cancer cells. In contrast, miR-9-5p rescues the function of LINC01116. miR-9-5p tends to bind STMN1 to preclude its expression. LINC01116 partly regulates STMN1 to target miR-9-5p (Bi et al., 2020; Figure 4). Liang et al. reported that LINC01116 enhanced the CRC cell proliferation, invasion and migration through interacting with EZH2 to potentiate methylation in the TPM1 promoter region to suppress the transcription of TPM1 (Figure 4). In addition, a previous study confirmed that LINC01116 was a regulator of ESR1 related to the proliferation of BC cells by sponging miR-145. In brief, LINC01116 actively stimulates the development of cell proliferation in many cancers by prompting miRNAs to mediate the expression of several proteins.

Chemotherapy is one of the primary treatment methods for several malignant tumors. However, the phenomenon of chemoresistance has increased, which has led to a serious dilemma in clinical treatment (Fatma et al., 2020; Jiang et al., 2020). Thus, there has been a great deal of research focusing on the molecular mechanisms of chemoresistance. Previous evidence has indicated that LINC01116 contributes to chemoresistance in some cancers (Li et al., 2021b), namely gefitinib and cisplatin resistance. Wang et al. (2020a) corroborated that LINC01116 contributed positively to the development of cisplatin resistance in LUAD, which depends on the EMT process (Figure 3). In contrast, LINC01116 silencing increases cisplatin sensitivity by mediating apoptosis and cell cycle distribution. Recent experiments have shed new light on the LINC01116-increasing effect of gefitinib resistance by regulating cell cycle through mediating IFI44 expression (Wang et al., 2020a; Figure 3). Furthermore, when LINC01116 is upregulated, the sensitivity of A549 cells to cisplatin is low. Conversely, silencing of LINC01116 generally leads to the inhibition of cisplatin resistance in A549 cells, via the stimulation of apoptosis and cell cycle arrest at the G0/G1 phase (Wang et al., 2020b). In summary, an abundance of chemoresistance mechanisms remain unclear. Thus, further studies are necessary.